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  • 1.
    Benrick, Anna
    et al.
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Chanclón, Belén
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Micallef, Peter
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Wu, Yanling
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Hadi, Laila
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Shelton, John M.
    Molecular Pathology Core, University of Texas Southwestern Medical Center, Dallas, TX, USA.
    Stener-Victorin, Elisabet
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Wernstedt Asterholm, Ingrid
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Adiponectin protects against development of metabolic disturbances in a PCOS mouse model2017In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 114, no 34, p. E7187-E7196, article id 201708854Article in journal (Refereed)
    Abstract [en]

    Adiponectin, together with adipocyte size, is the strongest factor associated with insulin resistance in women with polycystic ovary syndrome (PCOS). This study investigates the causal relationship between adiponectin levels and metabolic and reproductive functions in PCOS. Prepubertal mice overexpressing adiponectin from adipose tissue (APNtg), adiponectin knockouts (APNko), and their wild-type (WT) littermate mice were continuously exposed to placebo or dihydrotestosterone (DHT) to induce PCOS-like traits. As expected, DHT exposure led to reproductive dysfunction, as judged by continuous anestrus, smaller ovaries with a decreased number of corpus luteum, and an increased number of cystic/atretic follicles. A two-way between-groups analysis showed that there was a significant main effect for DHT exposure, but not for genotype, indicating adiponectin does not influence follicle development. Adiponectin had, however, some protective effects on ovarian function. Similar to in many women with PCOS, DHT exposure led to reduced adiponectin levels, larger adipocyte size, and reduced insulin sensitivity in WTs. APNtg mice remained metabolically healthy despite DHT exposure, while APNko-DHT mice were even more insulin resistant than their DHT-exposed littermate WTs. DHT exposure also reduced the mRNA expression of genes involved in metabolic pathways in gonadal adipose tissue of WT and APNko, but this effect of DHT was not observed in APNtg mice. Moreover, APNtg-DHT mice displayed increased pancreatic mRNA levels of insulin receptors, Pdx1 and Igf1R, suggesting adiponectin stimulates beta cell viability/hyperplasia in the context of PCOS. In conclusion, adiponectin improves metabolic health but has only minor effects on reproductive functions in this PCOS-like mouse model.

  • 2.
    Benrick, Anna
    et al.
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Kokosar, Milana
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Hu, Min
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Larsson, Martin
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Maliqueo, Manuel
    Endocrinology and Metabolism Laboratory, West Division, School of Medicine, University of Chile, Santiago, Chile.
    Marcondes, Rodrigo Rodrigues
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Disciplina de Ginecologia, Laboratório de Ginecologia Estrutural e Molecular (LIM 58), Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
    Soligo, Marzia
    Institute of Translational Pharmacology, Consiglio Nazionale delle Ricerche, Rome, Italy.
    Protto, Virginia
    Institute of Translational Pharmacology, Consiglio Nazionale delle Ricerche, Rome, Italy.
    Jerlhag, Elisabet
    Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Sazonova, Antonina
    Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Behre, Carl Johan
    Department of Cardiology, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Højlund, Kurt
    Department of Endocrinology, Odense University Hospital, Odense, Denmark.
    Thorén, Peter
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Autonomic nervous system activation mediates the increase in whole-body glucose uptake in response to electroacupuncture2017In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 31, no 8, p. 3288-3297Article in journal (Refereed)
    Abstract [en]

    A single bout of low-frequency electroacupuncture (EA) causing muscle contractions increases whole-body glucose uptake in insulin-resistant rats. We explored the underlying mechanism of this finding and whether it can be translated into clinical settings. Changes in glucose infusion rate (GIR) were measured by euglycemic-hyperinsulinemic clamp during and after 45 min of low-frequency EA in 21 overweight/obese women with polycystic ovary syndrome (PCOS) and 21 controls matched for age, weight, and body mass index (experiment 1) and in rats receiving autonomic receptor blockers (experiment 2). GIR was higher after EA in controls and women with PCOS. Plasma serotonin levels and homovanillic acid, markers of vagal activity, decreased in both controls and patients with PCOS. Adipose tissue expression of pro-nerve growth factor (proNGF) decreased, and the mature NGF/proNGF ratio increased after EA in PCOS, but not in controls, suggesting increased sympathetic-driven adipose tissue metabolism. Administration of alpha-/beta-adrenergic receptor blockers in rats blocked the increase in GIR in response to EA. Muscarinic and dopamine receptor antagonist also blocked the response but with slower onset. In conclusion, a single bout of EA increases whole-body glucose uptake by activation of the sympathetic and partly the parasympathetic nervous systems, which could have important clinical implications for the treatment of insulin resistance.

  • 3.
    Boberg, Lena
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Szekeres, Ferenc L. M.
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Arner, Anders
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Signaling and metabolic properties of fast and slow smooth muscle types from mice2018In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 470, no 4, p. 681-691Article in journal (Refereed)
    Abstract [en]

    This study aims to improve the classification of smooth muscle types to better understand their normal and pathological functional phenotypes. Four different smooth muscle tissues (aorta, muscular arteries, intestine, urinary bladder) with a 5-fold difference in maximal shortening velocity were obtained from mice and classified according to expression of the inserted myosin heavy chain (SMHC-B). Western blotting and quantitative PCR analyses were used to determine 15 metabolic and 8 cell signaling key components in each tissue. The slow muscle type (aorta) with a 12 times lower SMHC-B had 6-fold lower expression of the phosphatase subunit MYPT1, a 7-fold higher expression of Rhokinase 1, and a 3-fold higher expression of the PKC target CPI17, compared to the faster (urinary bladder) smooth muscle. The slow muscle had higher expression of components involved in glucose uptake and glycolysis (type 1 glucose transporter, 3 times; hexokinase, 13 times) and in gluconeogenesis (phosphoenolpyruvate carboxykinase, 43 times), but lower expression of the metabolic sensing AMP-activated kinase, alpha 2 isoform (5 times). The slow type also had higher expression of enzymes involved in lipid metabolism (hormone-sensitive lipase, 10 times; lipoprotein lipase, 13 times; fatty acid synthase, 6 times; type 2 acetyl-coenzyme A carboxylase, 8 times). We present a refined division of smooth muscle into muscle types based on the analysis of contractile, metabolic, and signaling components. Slow compared to fast smooth muscle has a lower expression of the deactivating phosphatase and upregulated Ca2+ sensitizing pathways and is more adapted for sustained glucose and lipid metabolism. © 2018 The Author(s)

  • 4.
    Borgström, Juliana
    University of Skövde, School of Bioscience.
    Cyclical Women: Menstrual Cycle Effects on Mood and Neuro-Cognitive Performance2019Independent thesis Basic level (degree of Bachelor), 15 credits / 22,5 HE creditsStudent thesis
    Abstract [en]

    During roughly forty years of a woman’s life-span, the fertile female human body prepares itself monthly for the possibility of pregnancy. Science has shown that the fluctuation of the sex steroids progesterone and estrogen have a crucial role in the female body's physiology, determining the menstrual cycle and its general phases. This biological dance of hormones governing the cycle influences a lot of physical, mental and cognitive aspects of life for a fertile ovulating woman. Although the question of whether these changes also affect women's cognitive performance is still unclear, some evidence has been gathered that could bring us closer to answers. Recent research findings show that this hormonal interplay might have a significant role in cognitive and psychological development - modulating brain activity, cognitive performance, higher cognition, emotional status, sensory processing, appetite and more. This thesis aims to uncover to what extent the menstrual cycle affects brain functions, neurobiology, mood, well-being and cognitive performance in menstruating cisgender women.

  • 5.
    Ekström, Anette
    et al.
    University of Skövde, School of Life Sciences.
    Widström, Ann-Marie
    Department of Woman and Child Health, Division of Reproductive and Perinatal Health Care, Karolinska Institutet, Stockholm, Sweden.
    Nissen, Eva
    University of Skövde, School of Life Sciences.
    Duration of Breastfeeding in Swedish Primiparous and Multiparous Women2003In: Journal of Human Lactation, ISSN 0890-3344, E-ISSN 1552-5732, Vol. 19, no 2, p. 172-178Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to describe the effects of sociodemographicfactors and maternity ward practices on the duration of breastfeedingin Swedish primiparas (n = 194) and multiparas (n = 294), consecutivelyselected from hospital birth files for 3 months, who respondedto a questionnaire 9 to 12 months after childbirth. The impactof sociodemographic data and maternity ward practices on exclusiveand any breastfeeding were examined. Smoking and supplementationwithout medical reasons influenced the duration of both exclusiveand any breastfeeding negatively, whereas early first breastfeedinginfluenced the duration of both exclusive and any breastfeedingpositively, and parity had no significant influence. Late hospitaldischarge influenced the duration of exclusive breastfeedingpositively, and higher maternal age influenced the durationof any breastfeeding positively. These variables altogetherexplained 11.4% (P <.001) of the variance in the durationof exclusive breastfeeding and 8.2% (P <.001) of the durationof any breastfeeding

  • 6.
    Fornes, Romina
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Maliqueo, Manuel
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Endocrinology and Metabolism Laboratory, Department of Medicine, West Division, University of Chile, Santiago, Chile.
    Hu, Min
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Hadi, Laila
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Jimenez-Andrade, Juan M.
    Unidad Académica Multidisciplinaria Reynosa Aztlán, Universidad Autónoma de Tamaulipas, Reynosa, Tamaulipas, Mexico.
    Ebefors, Kerstin
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Nyström, Jenny
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Labrie, Fernand
    Laval University Research Center in Molecular Endocrinology, Oncology and Human Genomics, CHUL Research Center, Quebec, Canada.
    Jansson, Thomas
    Department of Obstetrics & Gynecology, Division of Reproductive Sciences, University Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, 171 77, Stockholm, Sweden.
    The effect of androgen excess on maternal metabolism, placental function and fetal growth in obese dams2017In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 8066Article in journal (Refereed)
    Abstract [en]

    Pregnant women with polycystic ovary syndrome (PCOS) are often overweight or obese. To study the effects of maternal androgen excess in obese dams on metabolism, placental function and fetal growth, female C57Bl6J mice were fed a control (CD) or a high fat/high sucrose (HF/HS) diet for 4-10 weeks, and then mated. On gestational day (GD) 15.5-17.5, dams were injected with dihydrotestosterone (CD-DHT, HF/HS-DHT) or a vehicle (CD-Veh, HF/HS-Veh). HF/HS dams had higher fat content, both before mating and on GD18.5, with no difference in glucose homeostasis, whereas the insulin sensitivity was higher in DHT-exposed dams. Compared to the CD groups, the livers from HF/HS dams weighed more on GD18.5, the triglyceride content was higher, and there was a dysregulation of liver enzymes related to lipogenesis and higher mRNA expression of Fitm1. Fetuses from HF/HS-Veh dams had lower liver triglyceride content and mRNA expression of Srebf1c. Maternal DHT exposure, regardless of diet, decreased fetal liver Pparg mRNA expression and increased placental androgen receptor protein expression. Maternal diet-induced obesity, together with androgen excess, affects maternal and fetal liver function as demonstrated by increased triglyceride content and dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage.

  • 7.
    Fornes, Romina
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Solna.
    Manti, Maria
    Department of Physiology and Pharmacology, Karolinska Institutet, Solna.
    Qi, Xiaojuan
    Department of Physiology, Qiqihar Medical University, Qiqihar, China.
    Vorontsov, Egor
    Proteomics Core Facility, University of Gothenburg, Gothenburg.
    Sihlbom, Carina
    Proteomics Core Facility, University of Gothenburg, Gothenburg.
    Nyström, Jenny
    Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Jerlhag, Elisabet
    Department of Pharmacology, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Maliqueo, Manuel
    Endocrinology and Metabolism, Faculty of Medicine, West division, University of Chile, Santiago, Chile.
    Hirschberg, Angelica Lindén
    Division of Obstetrics and Gynecology, Karolinska University Hospital, Solna.
    Carlström, Mattias
    Department of Physiology and Pharmacology, Karolinska Institutet, Solna.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Solna.
    Mice exposed to maternal androgen excess and diet-induced obesity have altered phosphorylation of catechol-O-methyltransferase in the placenta and fetal liver2019In: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 43, p. 2176-2188Article in journal (Refereed)
    Abstract [en]

    Background/objectives: Maternal obesity together with androgen excess in mice negatively affects placental function and maternal and fetal liver function as demonstrated by increased triglyceride content with dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage. To identify changes in molecular pathways that might promote diseases in adulthood, we performed a global proteomic analysis using a liquid-chromatography/mass-spectrometry system to investigate total and phosphorylated proteins in the placenta and fetal liver in a mouse model that combines maternal obesity with maternal androgen excess. Methods: After ten weeks on a control diet (CD) or high fat/high sugar-diet, dams were mated with males fed the CD. Between gestational day (GD) 16.5 and GD 18.5, mice were injected with vehicle or dihydrotestosterone (DHT) and sacrificed at GD 18.5 prior to dissection of the placentas and fetal livers. Four pools of female placentas and fetal livers were subjected to a global proteomic analysis. Total and phosphorylated proteins were filtered by ANOVA q < 0.05, and this was followed by two-way ANOVA to determine the effect of maternal obesity and/or androgen exposure. Results: In placenta, phosphorylated ATP-citrate synthase was decreased due to maternal obesity, and phosphorylated catechol-O-methyltransferase (COMT) was differentially expressed due to the interaction between maternal diet and DHT exposure. In fetal liver, five total proteins and 48 proteins phosphorylated in one or more sites, were differentially expressed due to maternal obesity or androgen excess. In fetal liver, phosphorylated COMT expression was higher in fetus exposed to maternal obesity. Conclusion: These results suggest a common regulatory mechanism of catecholamine metabolism in the placenta and the fetal liver as demonstrated by higher phosphorylated COMT expression in the placenta and fetal liver from animals exposed to diet-induced maternal obesity and lower expression of phosphorylated COMT in animals exposed to maternal androgen excess. © 2019, Springer Nature Limited.

  • 8.
    Fritz, T.
    et al.
    Center for Family and Community Medicine, Karolinska Institutet, Huddinge, Sweden.
    Caidahl, K.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Krook, A.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lundström, P.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Mashili, F.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Osler, M.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Szekeres, Ferenc L. M.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Östenson, C. G.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Wändell, P.
    Center for Family and Community Medicine, Karolinska Institutet, Huddinge, Sweden.
    Zierath, J. R.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Effects of Nordic walking on cardiovascular risk factors in overweight individuals with type 2 diabetes, impaired or normal glucose tolerance2013In: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 29, no 1, p. 25-32Article in journal (Refereed)
    Abstract [en]

    Background Physical activity remains a valuable prevention for metabolic disease. The effects of Nordic walking on cardiovascular risk factors were determined in overweight individuals with normal or disturbed glucose regulation. Methods We included 213 individuals, aged 60 +/- 5.3 years and with body mass index (BMI) of 30.2 +/- 3.8 kg/m(2); of these, 128 had normal glucose tolerance (NGT), 35 had impaired glucose tolerance (IGT) and 50 had type 2 diabetes mellitus (T2DM). Participants were randomized to unaltered physical activity or to 5 h per week of Nordic walking with poles, for a 4-month period. Dietary habits were unaltered. BMI, waist circumference, blood pressure, glucose tolerance, clinical chemistry, maximal oxygen uptake (peak VO2) and self-reported physical activity (questionnaire) were assessed at the time of inclusion and after 4 months. The participants in the exercise-intervention group kept a walking diary. Results In the NGT exercise group, self-reported physical activity increased markedly, and body weight (-2.0 +/- 3.8 kg), BMI (-0.8 +/- 1.4 kg/m(2)) and waist circumference (- 4.9 +/- 4.4 cm) (mean +/- SD) decreased. Exercise power output (12.9 +/- 9.9 W) and peak VO2 (2.7 +/- 2.8 mL/kg/min) increased in the IGT exercise group. More cardiovascular risk factors were improved after exercise intervention in people with NGT compared with those with IGT or T2DM. Exercise capacity improved significantly in all three groups of participants who reported at least 80% compliance with the scheduled exercise. Conclusions Nordic walking improved anthropometric measurements and exercise capacity. However, unsupervised Nordic walking may not provide a sufficient increase in exercise intensity to achieve ultimate health-promoting benefits on the cardiovascular parameters assessed in this study, particularly for those with disturbed glucose regulation. Copyright (C) 2012 John Wiley & Sons, Ltd.

  • 9.
    Hellström Muhli, Ulla
    University of Skövde, School of Life Sciences.
    Refining the analytic lens to study elderly pain2008In: HCRC Newsletter, no 5, p. 4-4Article in journal (Other (popular science, discussion, etc.))
  • 10.
    Huang-Doran, Isabel
    et al.
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Bicknell, Louise S.
    Medical Research Council Human Genetics Unit, Institute of Genetics and Mo- lecular Medicine, Western General Hospital, Edinburgh, UK.
    Finucane, Francis M.
    Metabolic Research Unit, St. James Hospital, Trinity College, Dublin, Ireland.
    Rocha, Nuno
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Porter, Keith M.
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Tung, Y. C. Loraine
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Szekeres, Ferenc
    Integrative Physiology, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Krook, Anna
    Integrative Physiology, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Nolan, John J.
    Metabolic Research Unit, St. James Hospital, Trinity College, Dublin, Ireland.
    O'Driscoll, Mark
    Human DNA Damage Response Disorders Group, University of Sussex, Brighton, UK.
    Bober, Michael
    Division of Genetics, Department of Pediatrics, Alfred I. DuPont Hospital for Children, Wilmington, Delaware.
    O'Rahilly, Stephen
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Jackson, Andrew P.
    Medical Research Council Human Genetics Unit, Institute of Genetics and Mo- lecular Medicine, Western General Hospital, Edinburgh, UK.
    Semple, Robert K.
    Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
    Genetic Defects in Human Pericentrin Are Associated With Severe Insulin Resistance and Diabetes2011In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 60, no 3, p. 925-935Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE-Genetic defects in human pericentrin (PCNT), encoding the centrosomal protein pericentrin, cause a form of osteodysplastic primordial dwarfism that is sometimes reported to be associated with diabetes. We thus set out to determine the prevalence of diabetes and insulin resistance among patients with PCNT defects and examined the effects of pericentrin depletion on insulin action using 3T3-L1 adipocytes as a model system. RESEARCH DESIGN AND METHODS-A cross-sectional metabolic assessment of 21 patients with PCNT mutations was undertaken. Pericentrin expression in human tissues was profiled using quantitative real-time PCR. The effect of pericentrin knockdown on insulin action and adipogenesis in 3T3-L1 adipocytes was determined using Oil red 0 staining, gene-expression analysis, irnmunoblotting, and glucose uptake assays. Pericentrin expression and localization also was determined in skeletal muscle. RESULTS-Of 21 patients with genetic defects in PCNT, 18 had insulin resistance, which was severe in the majority of subjects. Ten subjects had confirmed diabetes (mean age of onset 15 years [range 5-28]), and 13 had metabolic dyslipidemia. All patients without insulin resistance were younger than 4 years old. Knockdown of pericentrin in adipocytes had no effect on proximal insulin signaling but produced a twofold impairment in insulin-stimulated glucose uptake, approximately commensurate with an associated defect in cell proliferation and adipogenesis. Pericentrin was highly expressed in human skeletal muscle, where it showed a perinuclear distribution. CONCLUSIONS-Severe insulin resistance and premature diabetes are common features of PCNT deficiency but are not congenital. Partial failure of adipocyte differentiation may contribute to this, but pericentrin deficiency does not impair proximal insulin action in adipocytes. Diabetes 60:925-935, 2011

  • 11.
    Kokosar, Milana
    et al.
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Perfilyev, Alexander
    Epigenetics and Diabetes, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Clinical Research Centre, Scania University Hospital, Malmö, Sweden.
    Nilsson, Emma
    Epigenetics and Diabetes, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Clinical Research Centre, Scania University Hospital, Malmö, Sweden.
    Källman, Thomas
    Department of Medical Biochemistry and Microbiology, NBIS - National Bioinformatics Infrastructure Sweden, SciLifeLab, Uppsala University, Uppsala, Sweden.
    Ohlsson, Claes
    Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Ling, Charlotte
    Epigenetics and Diabetes, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Clinical Research Centre, Scania University Hospital, Malmö, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden.
    A Single Bout of Electroacupuncture Remodels Epigenetic and Transcriptional Changes in Adipose Tissue in Polycystic Ovary Syndrome2018In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 1878Article in journal (Refereed)
    Abstract [en]

    A single bout of electroacupuncture results in muscle contractions and increased whole body glucose uptake in women with polycystic ovary syndrome (PCOS). Women with PCOS have transcriptional and epigenetic alterations in the adipose tissue and we hypothesized that electroacupuncture induces epigenetic and transcriptional changes to restore metabolic alterations. Twenty-one women with PCOS received a single bout of electroacupuncture, which increased the whole body glucose uptake. In subcutaneous adipose tissue biopsies, we identified treatment-induced expression changes of 2369 genes (Q < 0.05) and DNA methylation changes of 7055 individual genes (Q = 0.11). The largest increase in expression was observed for FOSB (2405%), and the largest decrease for LOC100128899 (54%). The most enriched pathways included Acute phase response signaling and LXR/RXR activation. The DNA methylation changes ranged from 1-16%, and 407 methylation sites correlated with gene expression. Among genes known to be differentially expressed in PCOS, electroacupuncture reversed the expression of 80 genes, including PPAR gamma and ADIPOR2. Changes in the expression of Nr4 alpha 2 and Junb are reversed by adrenergic blockers in rats demonstrating that changes in gene expression, in part, is due to activation of the sympathetic nervous system. In conclusion, low-frequency electroacupuncture with muscle contractions remodels epigenetic and transcriptional changes that elicit metabolic improvement.

  • 12.
    Kulkarni, Sameer S.
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Karlsson, Håkan K. R.
    Karolinska Institutet, Stockholm, Sweden.
    Szekeres, Ferenc
    Karolinska Institutet, Stockholm, Sweden.
    Chibalin, Alexander V.
    Karolinska Institutet, Stockholm, Sweden.
    Krook, Anna
    Karolinska Institutet, Stockholm, Sweden.
    Zierath, Juleen R.
    Karolinska Institutet, Stockholm, Sweden.
    Suppression of 5 '-Nucleotidase Enzymes Promotes AMP-activated Protein Kinase (AMPK) Phosphorylation and Metabolism in Human and Mouse Skeletal Muscle2011In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 286, no 40, p. 34567-34574Article in journal (Refereed)
    Abstract [en]

    The 5'-nucleotidase (NT5) family of enzyme dephosphorylates non-cyclic nucleoside monophosphates to produce nucleosides and inorganic phosphates. We hypothesized that gene silencing of NT5 enzymes to increase the intracellular availability of AMP would increase AMP-activated protein kinase (AMPK) activity and metabolism. We determined the role of cytosolic NT5 in metabolic responses linked to the development of insulin resistance in obesity and type 2 diabetes. Using siRNA to silence NT5C2 expression in cultured human myotubes, we observed a 2-fold increase in the AMP/ATP ratio, a 2.4-fold increase in AMPK phosphorylation (Thr(172)), and a 2.8-fold increase in acetyl-CoA carboxylase phosphorylation (Ser(79)) (p<0.05). siRNA silencing of NT5C2 expression increased palmitate oxidation by 2-fold in the absence and by 8-fold in the presence of 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside. This was paralleled by an increase in glucose transport and a decrease in glucose oxidation, incorporation into glycogen, and lactate release from NT5C2-depleted myotubes. Gene silencing of NT5C1A by shRNA injection and electroporation in mouse tibialis anterior muscle reduced protein content (60%; p<0.05) and increased phosphorylation of AMPK (60%; p<0.05) and acetyl-CoA carboxylase (50%; p<0.05) and glucose uptake (20%; p<0.05). Endogenous expression of NT5C enzymes inhibited basal lipid oxidation and glucose transport in skeletal muscle. Reduction of 5'-nucleotidase expression or activity may promote metabolic flexibility in type 2 diabetes.

  • 13.
    Maliqueo, Manuel
    et al.
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden / Laboratorio de Endocrinología y Metabolismo, Departamento de Medicina Occidente, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
    Benrick, Anna
    University of Skövde, School of Health and Education. Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Rodrigues Marcondes, Rodrigo
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden / Laboratório de Ginecologia Estrutural e Molecular (LIM 58), Disciplina de Ginecologia, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
    Johansson, Julia
    Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Sun, Miao
    Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden / Department of Obstetrics and Gynecology, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, China.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Acupuncture does not ameliorate metabolic disturbances in the P450 aromatase inhibitor-induced rat model of polycystic ovary syndrome2017In: Experimental Physiology, ISSN 0958-0670, E-ISSN 1469-445X, Vol. 102, no 1, p. 113-127Article in journal (Refereed)
    Abstract [en]

    Low-frequency electroacupuncture restores sex steroid synthesis and sympathetic activity in women with polycystic ovary syndrome, which may improve its metabolic disturbances likely by modulating sympathetic nerve activity or sex steroid synthesis. We investigated whether low-frequency electroacupuncture regulates the metabolic function to the same extent as treatment with estradiol or -adrenergic blocking in a rat model of polycystic ovary syndrome induced by a P450 aromatase inhibitor (letrozole). Letrozole (β00 μg per day) or placebo pellets were implanted in pre-pubertal Wistar rats. Six weeks thereafter, rats were treated for 5–6 weeks with: low-frequency electroacupuncture (5 days per week), a -adrenergic blocker (propranolol hydrochloride, 0.1 mg kg-1) (5 days per week), or 17-estradiol (β.0 μg) every fourth day. Body weight development, body composition, locomotor activity, insulin sensitivity, tissue specific glucose uptake, lipid profile, adipocyte size, adiponectin and insulin serum concentrations, and gene expression in inguinal fat were measured. All treatments increased circulating levels of LDL-cholesterol. Estradiol treatment restored locomotor activity and increased insulin sensitivity but did not modify the glucose uptake in muscle and fat. An upregulation of genes related to insulin sensitivity and downregulation of genes related to adipogenesis were observed in subcutaneous adipose tissue from rats exposed to letrozole. Only estradiol treatment normalized the expression of these genes. In conclusions, low-frequency electroacupuncture increased LDL-cholesterol without affecting the insulin sensitivity or adipose tissue function, which could suggest effects on hepatic lipid regulation probably mediated by estradiol action or -adrenergic pathway.

  • 14.
    Manti, Maria
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Fornes, Romina
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Pironti, Gianluigi
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    McCann Haworth, Sarah
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Zhengbing, Zhuge
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Carlström, Mattias
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Daniel
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Heart and Vascular Theme, Heart Failure and Congenital Heart Disease Section, Karolinska University Hospital, Stockholm, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Maternal androgen excess induces cardiac hypertrophy and left ventricular dysfunction in female mice offspring2019In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, article id 31382275Article in journal (Refereed)
  • 15.
    Manti, Maria
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Fornes, Romina
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Qi, Xiaojuan
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Department of Physiology, Qiqihar Medical University, Qiqihar, China.
    Folmerz, Elin
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lindén Hirschberg, Angelica
    Department of Obstetrics and Gynecology, Karolinska Institutet, Stockholm, Sweden.
    de Castro Barbosa, Thais
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Maliqueo, Manuel
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / West Division, Endocrinology and Metabolism Laboratory, School of Medicine, University of Chile, Santiago, Chile.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring2018In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 32, no 8, p. 4158-4171Article in journal (Refereed)
    Abstract [en]

    Maternal polycystic ovary syndrome (PCOS), a condition associated with hyperandrogenism, is suggested to increase anxiety-like behavior in the offspring. Because PCOS is closely linked to obesity, we investigated the impact of an adverse hormonal or metabolic maternal environment and offspring obesity on anxiety in the offspring. The obese PCOS phenotype was induced by chronic high-fat-high-sucrose (HFHS) consumption together with prenatal dihydrotestosterone exposure in mouse dams. Anxiety-like behavior was assessed in adult offspring with the elevated-plus maze and open-field tests. The influence of maternal androgens and maternal and offspring diet on genes implicated in anxiety were analyzed in the amygdala and hypothalamus with real-time PCR ( n = 47). Independent of diet, female offspring exposed to maternal androgens were more anxious and displayed up-regulation of adrenoceptor α 1B in the amygdala and up-regulation of hypothalamic corticotropin-releasing hormone ( Crh). By contrast, male offspring exposed to a HFHS maternal diet had increased anxiety-like behavior and showed up-regulation of epigenetic markers in the amygdala and up-regulation of hypothalamic Crh. Overall, there were substantial sex differences in gene expression in the brain. These findings provide novel insight into how maternal androgens and obesity exert sex-specific effects on behavior and gene expression in the offspring of a PCOS mouse model.-Manti, M., Fornes, R., Qi, X., Folmerz, E., Lindén Hirschberg, A., de Castro Barbosa, T., Maliqueo, M., Benrick, A., Stener-Victorin, E. Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring.

  • 16.
    Mudry, Jonathan M.
    et al.
    Section for Integrative Physiology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Massart, Julie
    Section for Integrative Physiology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Szekeres, Ferenc L. M.
    Section for Integrative Physiology, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Krook, Anna
    Section for Integrative Physiology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden / Section for Integrative Physiology, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    TWIST1 and TWIST2 regulate glycogen storage and inflammatory genes in skeletal muscle2015In: Journal of Endocrinology, ISSN 0022-0795, E-ISSN 1479-6805, Vol. 224, no 3, p. 303-313Article in journal (Refereed)
    Abstract [en]

    TWIST proteins are important for development of embryonic skeletal muscle and play a role in the metabolism of tumor and white adipose tissue. The impact of TWIST on metabolism in skeletal muscle is incompletely studied. Our aim was to assess the impact of TWIST1 and TWIST2 overexpression on glucose and lipid metabolism. In intact mouse muscle, overexpression of Twist reduced total glycogen content without altering glucose uptake. Expression of TWIST1 or TWIST2 reduced Pdk4 mRNA, while increasing mRNA levels of Il6, Tnf alpha, and Il1 beta. Phosphorylation of AKT was increased and protein abundance of acetyl CoA carboxylase ( ACC) was decreased in skeletal muscle overexpressing TWIST1 or TWIST2. Glycogen synthesis and fatty acid oxidation remained stable in C2C12 cells overexpressing TWIST1 or TWIST2. Finally, skeletal muscle mRNA levels remain unaltered in ob/ob mice, type 2 diabetic patients, or in healthy subjects before and after 3 months of exercise training. Collectively, our results indicate that TWIST1 and TWIST2 are expressed in skeletal muscle. Overexpression of these proteins impacts proteins in metabolic pathways and mRNA level of cytokines. However, skeletal muscle levels of TWIST transcripts are unaltered in metabolic diseases.

  • 17.
    Nilsson, Emma
    et al.
    Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Skåne University Hospital, Malmö, Sweden.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Kokosar, Milana
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Krook, Anna
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lindgren, Eva
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Källman, Thomas
    Department of Medical Biochemistry and Microbiology, National Bioinformatics Infrastructure Sweden, SciLifeLab, Uppsala University, Uppsala, Sweden.
    Martis, Mihaela M.
    National Bioinformatics Infrastructure Sweden, Division of Cell Biology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Højlund, Kurt
    Department of Endocrinology, Odense University, Odense C, Denmark.
    Ling, Charlotte
    Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Skåne University Hospital, Malmö, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Transcriptional and Epigenetic Changes Influencing Skeletal Muscle Metabolism in Women With Polycystic Ovary Syndrome2018In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 103, no 12, p. 4465-4477Article in journal (Refereed)
    Abstract [en]

    Context: Insulin resistance in skeletal muscle is a major risk factor for the development of type 2 diabetes in women with polycystic ovary syndrome (PCOS). Despite this, the mechanisms underlying insulin resistance in PCOS are largely unknown. Objective: To investigate the genome-wide DNA methylation and gene expression patterns in skeletal muscle from women with PCOS and controls and relate them to phenotypic variations. Design/Participants: In a case-control study, skeletal muscle biopsies from women with PCOS (n = 17) and age-, weight-, and body mass index. matched controls (n = 14) were analyzed by array-based DNA methylation and mRNA expression profiling. Results: Eighty-five unique transcripts were differentially expressed in muscle from women with PCOS vs controls, including DYRK1A, SYNPO2, SCP2, and NAMPT. Furthermore, women with PCOS had reduced expression of genes involved in immune system pathways. Two CpG sites showed differential DNA methylation after correction for multiple testing. However, an mRNA expression of similar to 30% of the differentially expressed genes correlated with DNA methylation levels of CpG sites in or near the gene. Functional follow-up studies demonstrated that KLF10 is under transcriptional control of insulin, where insulin promotes glycogen accumulation in myotubes of human muscle cells. Testosterone downregulates the expression levels of COL1A1 and MAP2K6. Conclusion: PCOS is associated with aberrant skeletal muscle gene expression with dysregulated pathways. Furthermore, we identified specific changes in muscle DNA methylation that may affect gene expression. This study showed that women with PCOS have epigenetic and transcriptional changes in skeletal muscle that, in part, can explain the metabolic abnormalities seen in these women.

  • 18.
    Nilsson, Håkan
    University of Skövde, School of Technology and Society.
    Hjärnans signalsystem metodologi och funktion2007In: Neurodidaktik: Om hjärnvägar och knutpunkter / [ed] Aadu Ott & Carl E. Olivestam, Göteborg: Institutionen för pedagogik och didaktik, Neurodidaktiska kollegiet, Göteborgs universitet , 2007, p. 19-29Chapter in book (Other academic)
  • 19.
    Olofsson, Peder S.
    et al.
    Center for Bioelectronic Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden / Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Steinberg, Benjamin E.
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA / The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario, Canada.
    Sobbi, Roozbeh
    Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.
    Cox, Maureen A.
    The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario, Canada.
    Ahmed, Mohamed N.
    Center for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Oswald, Michaela
    Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Szekeres, Ferenc
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Hanes, William M.
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Introini, Andrea
    Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Liu, Shu Fang
    Center for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Holodick, Nichol E.
    Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Rothstein, Thomas L.
    Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Lövdahl, Cecilia
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Chavan, Sangeeta S.
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Yang, Huan
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Pavlov, Valentin A.
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Broliden, Kristina
    Department of Medicine, Solna, Unit of Infectious Diseases, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Andersson, Ulf
    Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
    Diamond, Betty
    The Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Miller, Edmund J.
    Center for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Arner, Anders
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Gregersen, Peter K.
    Robert S. Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Backx, Peter H.
    Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada / Department of Biology, York University, Toronto, Ontario, Canada.
    Mak, Tak W.
    The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario, Canada.
    Tracey, Kevin J.
    Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
    Blood pressure regulation by CD4lymphocytes expressing choline acetyltransferase2016In: Nature Biotechnology, ISSN 1087-0156, E-ISSN 1546-1696, Vol. 34, no 10, p. 1066-1071Article in journal (Refereed)
    Abstract [en]

    Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4(+) T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals(1). Here we show that these CD4(+)CD44(hi)CD62L(Io) T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T-ChAT). Mice lacking ChAT expression in CD4(+) cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT(ChAT)) decreased blood pressure when infused into mice. Co-incubation of JT(ChAT) and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T-ChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation.

  • 20.
    Rehn, Therese
    et al.
    Swedish University of Agricultural Sciences, Department of Animal Environment and Health, Uppsala, Sweden.
    Handlin, Linda
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Uvnäs-Moberg, Kerstin
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Swedish University of Agricultural Sciences, Department of Animal Environment and Health, Uppsala, Sweden.
    Keeling, Linda J.
    Swedish University of Agricultural Sciences, Department of Animal Environment and Health, Uppsala, Sweden.
    Dogs' endocrine and behavioural responses at reunion are affected by how the human initiates contact2014In: Physiology and Behavior, ISSN 0031-9384, E-ISSN 1873-507X, Vol. 124, p. 45-53Article in journal (Refereed)
  • 21.
    Rune, A.
    et al.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Salehzadeh, F.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Szekeres, F.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Kuhn, I.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Osler, M. E.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Al-Khalili, L.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Evidence against a sexual dimorphism in glucose and fatty acid metabolism in skeletal muscle cultures from age-matched men and post-menopausal women2009In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 197, no 3, p. 207-215Article in journal (Refereed)
    Abstract [en]

    Aim: In vivo whole body differences in glucose/lipid metabolism exist between men and women. Thus, we tested the hypothesis that intrinsic sex differences exist in skeletal muscle gene expression and glucose/lipid metabolism using cultured myotubes. Methods: Myotube cultures were prepared for gene expression and metabolic studies from vastus lateralis skeletal muscle biopsies obtained from age-matched men (n = 11; 59 +/- 2 years) and post-menopausal women (n = 10; 60 +/- 1 years). Results: mRNA expression of several genes involved in glucose and lipid metabolism was higher in skeletal muscle biopsies from female vs. male donors, but unaltered between the sexes in cultured myotubes. Basal and insulin-stimulated glucose uptake, as well as glucose incorporation into glycogen, was similar in myotube cultures derived from male vs. female donors. In males vs. females, insulin increased glucose uptake (1.3 +/- 0.1 vs. 1.5 +/- 0.1-fold respectively) and incorporation into glycogen (2.3 +/- 0.3 vs. 2.0 +/- 0.3-fold respectively) to the same extent. Basal fatty acid oxidation and rate of uptake/accumulation was similar between sexes. In response to the 5'AMP-activated protein kinase activator AICAR, lipid oxidation was increased to the same extent in myotubes established from male vs. female donors (1.6 +/- 0.6 vs. 2.0 +/- 0.3-fold respectively). Moreover, the AICAR-induced rate of uptake/accumulation was similar between sexes. Conclusion: Differences in metabolic parameters and gene expression profiles between age-matched men and post-menopausal women noted in vivo are not observed in cultured human skeletal muscle cells. Thus, the sexual dimorphism in glucose and lipid metabolism is likely a consequence of systemic whole body factors, rather than intrinsic differences in the skeletal muscle proper.

  • 22.
    Stener-Victorin, Elisabet
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Benrick, Anna
    University of Skövde, School of Health and Education. Department of Physiology, Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Fornes, Romina
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Maliqueo, Manuel
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Endocrinology and Metabolism Laboratory, West division, School of Medicine, University of Chile, Santiago, Chile.
    Acupuncture2018In: Infertility in Women with Polycystic Ovary Syndrome: Pathogenesis and Management / [ed] Stefano Palomba, Springer, 2018, p. 227-245Chapter in book (Refereed)
    Abstract [en]

    Acupuncture involving insertion of thin sterile needles into the skin, muscles, and fibrous/fat tissues is a part of traditional Chinese medicine (TCM). Western medical acupuncture described in this chapter is an adaptation of Chinese acupuncture using current knowledge of anatomy, physiology, pathology, and evidence-based medicine, instead of using concepts such as meridiansyin/yang, and circulation of qi. This chapter describes the use of acupuncture in the treatment of women with polycystic ovary syndrome (PCOS) from a western medical approach including potential mechanism of action, experimental data as well as clinical data.

  • 23.
    Stener-Victorin, Elisabet
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Manti, Maria
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Fornes, Romina
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Centre for Translational Microbiome Research (CTMR), Department of Microbiology, Tumor and Cell biology, Karolinska Institutet, Stockholm, Sweden.
    Risal, Sanjiv
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lu, Haojiang
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Benrick, Anna
    University of Skövde, School of Health and Education. University of Skövde, Health and Education. Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Origins and Impact of Psychological Traits in Polycystic Ovary Syndrome2019In: Medical sciences, ISSN 2076-3271, Vol. 7, no 8, article id 86Article, review/survey (Refereed)
  • 24.
    Synnergren, Jane
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Améen, Caroline
    Cellartis, Gothenburg, Sweden.
    Lindahl, Anders
    Dept of Clinical Chemistry/Transfusion Medicine, Sahlgrenska University Hospital, Sweden.
    Olsson, Björn
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Sartipy, Peter
    Cellartis, Gothenburg, Sweden .
    Expression of microRNAs and their target mRNAs in human stem cell-derived cardiomyocyte clusters and in heart tissue2011In: Physiological Genomics, ISSN 1094-8341, E-ISSN 1531-2267, Vol. 43, no 10, p. 581-594Article in journal (Refereed)
    Abstract [en]

    Recent studies have shown that microRNAs (miRNAs) act as posttranscriptional regulators and that they play important roles during heart development and in cardiac function. Thus, they may provide new means of altering stem cell fate and differentiation processes. However, information about the correlation between global miRNA and mRNA expression in cardiomyocyte clusters (CMCs) derived from human embryonic stem cells (hESC) and in fetal and adult heart tissue is lacking. In the present study the global miRNA and mRNA expression in hESC-derived CMCs and in fetal and adult heart tissue was investigated in parallel using microarrays. Target genes for the differentially expressed miRNAs were predicted using computational methods, and the concordance in miRNA expression and mRNA levels of potential target genes was determined across the experimental samples. The biology of the predicted target genes was further explored regarding their molecular functions and involvement in known regulatory pathways. A clear correlation between the global miRNA expression and corresponding target mRNA expression was observed. Using three different sources of cardiac tissue-like samples, we defined the similarities between in vitro hESC-derived CMCs and their in vivo counterparts. The results are in line with previously reported observations that miRNAs repress mRNA expression and additionally identify a number of novel miRNAs with potential important roles in human cardiac tissue. The concordant miRNA expression pattern observed among all the cardiac tissue-like samples analyzed here provide a starting point for future ambitious studies aiming towards assessment of the functional roles of specific miRNAs during cardiomyocyte differentiation.

  • 25.
    Szekeres, Ferenc
    et al.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Chadt, Alexandra
    German Institute of Human Nutrition, Potsdam-Rehbruecke, Department of Pharmacology, Nuthetal, Germany.
    Tom, Robby Z.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Deshmukh, Atul S.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Chibalin, Alexander V.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Björnholm, Marie
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Al-Hasani, Hadi
    German Institute of Human Nutrition, Potsdam-Rehbruecke, Department of Pharmacology, Nuthetal, Germany.
    Zierath, Juleen R.
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden / Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    The Rab-GTPase-activating protein TBC1D1 regulates skeletal muscle glucose metabolism2012In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 303, no 4, p. E524-E533Article in journal (Refereed)
    Abstract [en]

    Szekeres F, Chadt A, Tom RZ, Deshmukh AS, Chibalin AV, Bjornholm M, Al-Hasani H, Zierath JR. The Rab-GTPase-activating protein TBC1D1 regulates skeletal muscle glucose metabolism. Am J Physiol Endocrinol Metab 303: E524-E533, 2012. First published June 12, 2012; doi:10.1152/ajpendo.00605.2011.-The Rab-GTPase-activating protein TBC1D1 has emerged as a novel candidate involved in metabolic regulation. Our aim was to determine whether TBC1D1 is involved in insulin as well as energy-sensing signals controlling skeletal muscle metabolism. TBC1D1-deficient congenic B6.SJL-Nob1.10 (Nob1.10(SJL)) and wild-type littermates were studied. Glucose and insulin tolerance, glucose utilization, hepatic glucose production, and tissue-specific insulin-mediated glucose uptake were determined. The effect of insulin, AICAR, or contraction on glucose transport was studied in isolated skeletal muscle. Glucose and insulin tolerance tests were normal in TBC1D1-deficient Nob1.10(SJL) mice, yet the 4-h-fasted insulin concentration was increased. Insulin-stimulated peripheral glucose utilization during a euglycemic hyperinsulinemic clamp was similar between genotypes, whereas the suppression of hepatic glucose production was increased in TBC1D1-deficient mice. In isolated extensor digitorum longus (EDL) but not soleus muscle, glucose transport in response to insulin, AICAR, or contraction was impaired by TBC1D1 deficiency. The reduction in glucose transport in EDL muscle from TBC1D1-deficient Nob1.10(SJL) mice may be explained partly by a 50% reduction in GLUT4 protein, since proximal signaling at the level of Akt, AMPK, and acetyl-CoA carboxylase (ACC) was unaltered. Paradoxically, in vivo insulin-stimulated 2-deoxyglucose uptake was increased in EDL and tibialis anterior muscle from TBC1D1-deficient mice. In conclusion, TBC1D1 plays a role in regulation of glucose metabolism in skeletal muscle. Moreover, functional TBC1D1 is required for AICAR- or contraction-induced metabolic responses, implicating a role in energy-sensing signals.

  • 26.
    Szekeres, Ferenc
    et al.
    Karolinska Institutet, Department of physiology and pharmacology, Division of genetic physiology, Stockholm, Sweden.
    Walum, Erik
    Glucox Biotech AB, Stockholm, Sweden.
    Wikström, P.
    Glucox Biotech AB, Stockholm, Sweden.
    Arner, A.
    Karolinska Institutet, Department of physiology and pharmacology, Division of genetic physiology, Stockholm, Sweden.
    A small molecule inhibitor of Nox2 and Nox4 improves cardiac contractility after ischemia-reperfusion in the mouse heart2014In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 211, no s696, p. 93-93Article in journal (Refereed)
  • 27.
    Uvnäs-Moberg, Kerstin
    et al.
    Department of Animal Environment and Health, Swedish University of Agricultural Sciences, Skara, Sweden.
    Handlin, Linda
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Kendall-Tackett, Kathleen
    Texas Tech University School of Medicine, Amarillo, TX, USA.
    Petersson, Maria
    Department of Molecular Medicine and Surgery, Endocrine and Diabetes Unit, Karolinska Institutet, Sweden.
    Oxytocin is a principal hormone that exerts part of its effects by active fragments2019In: Medical Hypotheses, ISSN 0306-9877, E-ISSN 1532-2777, Vol. 133, p. 1-9, article id 109394Article in journal (Refereed)
    Abstract [en]

    Oxytocin is a nonapeptide consisting of a cyclic six amino-acid structure and a tail of three amino acids. It was originally known for its ability to induce milk ejection and to stimulate uterine contractions. More recently, oxytocin has been shown to stimulate social behaviors, and exert pain-relieving, anti-stress/anti-inflammatory and restorative effects. We hypothesize that oxytocin is a principal hormone that, in part, exerts its effects after degradation to active fragments with more specific effect profiles. Experimental findings on rats show that administered oxytocin exerts biphasic effects. For example, after an initial increase in pain threshold, a second more long-lasting increase follows. Blood pressure and cortisol levels initially increase and then reverse into a long-lasting decrease in blood pressure and cortisol. Whereas the initial effects are, the second-phase effects are not blocked by an oxytocin antagonist, but by an opioid mu-antagonist and by an alpha 2-adrenoreceptor antagonist, respectively, suggesting that other receptors are involved. Repeated administration of oxytocin induces multiple anti-stress effects, which are mediated by alpha 2-adrenoreceptors. Repeated administration of linear oxytocin and linear oxytocin fragments with a retained C-terminal reduce spontaneous motor activity, a sedative or anti-stress effect, suggesting that alpha 2-adrenoreceptors have been activated. In contrast, linear mid-fragments stimulate motor activity. Low-intensity stimulation of cutaneous nerves in rats, as well as breastfeeding and skin-to-skin contact between mothers and babies, trigger immediate anti-stress effects. Some of these effects are likely caused by open ring/linear C-terminal fragments activating alpha 2-adrenoreceptors. Oxytocin fragments may be pre-formed and released in the brain or created by metabolic conversion of the principal hormone oxytocin in the central nervous system. Oxytocin and its fragments may also be released from peripheral sites, such as peripheral nerves, the gastrointestinal tract, and blood vessels in response to decreased sympathetic or increased parasympathetic nervous tone. Smaller fragments of oxytocin produced in the periphery may easily pass the blood-brain barrier to induce effects in the brain. In conclusion, oxytocin is linked to many different, sometimes opposite effects. The intact cyclic molecule may act to initiate social interaction and associated psychophysiological effects, whereas linear oxytocin and C-terminal fragments may induce relaxation and anti-stress effects following social interaction. In this way, the principal hormone oxytocin and its fragments may take part in a behavioral sequence, ranging from approach and interaction to calm and relaxation. Linear fragments, with an exposed cysteine-residue, may exert anti-inflammatory and antioxidant effects and thereby contribute to the health-promoting effects of oxytocin. 

  • 28.
    Warrén-Stomberg, Margareta
    et al.
    University of Skövde, School of Life Sciences.
    Lorentzen, Per
    Skaraborgs Hospital, Skövde, Sweden.
    Joelsson, Håkan
    Skaraborgs Hospital, Skövde, Sweden.
    Lindquist, Helene
    Skaraborgs Hospital, Skövde, Sweden.
    Haljamäe, Hengo
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Postoperative pain management on surgical wards: impact of database documentation of anesthesia organized services2003In: Pain Management Nursing, ISSN 1524-9042, E-ISSN 1532-8635, Vol. 4, no 4, p. 155-164Article in journal (Refereed)
    Abstract [en]

    Postoperative pain management (POPM) should be based on an organization exploiting existing expertise and documenting the outcome of the POPM in each individual patient. The aims of the present study were to evaluate the adequacy of database documentation of POPM of an anesthesia organized, nurse-based, anesthesiologist-supervised acute pain service (APS) on surgical wards and to assess to what extent the information obtained was continuously used to improve practice. From 2890 registered cases in the database (patient controlled analgesia, n = 1975; epidural analgesia [EDA], n = 915), a homogeneous two-year sample of documentation charts from use of EDA for POPM in connection with major, open, abdominal surgical procedures (n = 381) was chosen for detailed analysis. The data charts contained information on patient data, drug dosage, total amount of infused drug, duration of EDA treatment, occurrence of side effects, and patient’s level of satisfaction. The database information was easily accessible making assessment of relevant aspects of the routines, including associations between analgesic technique, patient related factors, and satisfaction with the services, immediately available. Only 58% of the data charts were properly completed and fed into the database but the clinical safety of the missing nondatabase documented sample was not found jeopardized. Although the database documentation routines were considered to fulfill basic requirements of data collection and monitoring of the appropriateness of POPM, they were not found to function optimally. The reason seemed to be inadequate feedback of information between the parties involved in the POPM services. The present study stresses the importance of establishing routines for adequate, continuous feedback of recorded audit data from the APS team to the surgical wards for the maintenance of a high level of compliance with accepted guidelines.

  • 29.
    Warrén-Stomberg, Margareta
    et al.
    University of Skövde, School of Life Sciences.
    Sjöström, Björn
    University of Skövde, School of Life Sciences.
    Haljamae, Hengo
    Routine intra-operative assessment of pain and/or depth of anaesthesia by nurse anaesthetists in clinical practice2001In: Journal of Clinical Nursing, ISSN 1365-2702, Vol. 19, no 4, p. 429-436Article in journal (Refereed)
    Abstract [en]

    • Patient safety and comfort during general anaesthesia and surgery are to a considerable extent dependent on the capability of anaesthesia personnel to interpret directly monitored as well as indirect clinical signs of pain and/or depth of anaesthesia.

    • The aim of the present study was to evaluate how nurse anaesthetists in their clinical routine work assess and interpret intra-operative responses evoked by pain stimuli and/or insufficient depth of anaesthesia.

    • A questionnaire was designed to assess the perceived relevance and validity of cardiovascular, respiratory, mucocutaneous, eye-associated, and muscular responses for routine assessment of intra-operative pain and/or insufficient depth of anaesthesia in patients undergoing surgery under general anaesthesia.

    • Data were obtained from 223 nurse anaesthetists working at nine different university anaesthesia departments in Sweden.

    • A number of significant indicators for pain and depth of anaesthesia could be identified for spontaneously breathing as well as for mechanically ventilated patients. No variable was considered entirely specific for either intra-operative pain or depth of anaesthesia. Changes in breathing rate/volume, central haemodynamics (BP, HR), lacrimation, and presence of moist and sticky skin were given higher score values as indicators of pain than as indicators of depth of anaesthesia. Occurrence of grimaces, attempted movements, and presence of non-centred pupils were variables considered more indicative of insufficient depth of anaesthesia than intra-operative pain.

    • In conclusion, it is obvious from the present data that indirect physiological signs of intra-operative pain and depth of anaesthesia are still considered of importance by Swedish anaesthesia nurses in the anaesthetic management of surgical patients.

  • 30.
    Warrén-Stomberg, Margareta
    et al.
    University of Skövde, Department of Health Sciences.
    Sjöström, Björn
    University of Skövde, Department of Health Sciences. Göteborg University.
    Haljamäe, Hengo
    Sahlgrenska University Hospital, Göteborg.
    Assessing Pain Responses During General Anesthesia2001In: AANA Journal, ISSN 0094-6354, Vol. 69, no 3, p. 218-222Article in journal (Refereed)
    Abstract [en]

    Major technical and pharmacological achievements in recent years have greatly influenced the practice of anesthesia. Clinical signs related to the main aspects of anesthesia, i.e., hypnosis, analgesia, and muscular relaxation, are increasingly obtainable from variables supplied by the monitoring equipment. It is not known, however, to what extent more indirect, patient-associated clinical signs of pain/depth of anesthesia are still considered of importance and relied on in the intraoperative management of surgical patients. The aims of the present study were to assess what clinical signs, indirect as well as monitor-derived, are considered indicative of intraoperative pain or depth of anesthesia by nurse anesthetists during general anesthesia. In connection with anesthetic management of surgical patients, Swedish nurse anesthetists (N = 40) were interviewed about clinical signs that they routinely assessed and were asked if the observed signs were considered indicative mainly of intraoperative pain or depth of anesthesia. It was found that skin-associated responses (temperature, color, moisture/stickiness) were commonly considered to indicate intraoperative pain rather than depth of anesthesia. Respiratory movements, eye reactions, and circulatory responses were considered to be indicative of either pain or insufficient depth of anesthesia. The present data indicate that indirect physiological signs are still considered of major importance by anesthesia nurses during the anesthetic management of surgical patients.

  • 31.
    Warrén-Stomberg, Margareta
    et al.
    University of Skövde, School of Life Sciences. University of Göteborg.
    Sjöström, Björn
    University of Skövde, School of Life Sciences.
    Haljamäe, Hengo
    Sahlgrenska University Hosptial, University of Göteborg.
    The role of the nurse anesthetist in the planning of postoperative pain management2003In: AANA Journal, ISSN 0094-6354, Vol. 71, no 3, p. 197-202Article in journal (Refereed)
    Abstract [en]

    Adequate pain relief after surgery is essential for avoiding pain-associated stress and patient comfort in the postoperative period. The Swedish nurse anesthetist has an important role in the intraoperative management of the surgical patient by assessing and moderating individual physiological response evoked by surgical stimuli during general anesthesia. The extent to which knowledge of specific individual response patterns are used to plan postoperative pain management is unknown. The aim of the present study was to assess the role of the nurse anesthetist in planning early postoperative pain management for surgical patients. Nurse anesthetists (N = 101) at 4 academic hospitals in Sweden responded to a questionnaire focusing, in addition to demographic data, on intraoperative routines for postoperative pain management, perceived clinical relevance of used routines, personal involvement (in addition to existing routines) in postoperative pain management, factors influencing pain alleviation requirements, and the potential role of the nurse anesthetist for improved postoperative pain management. We found that type of anesthesia and type of surgical procedure were both factors considered important for postoperative pain management. A majority of the participants believed that pain management approaches were not appropriately individualized to the patient.

  • 32.
    Warrén-Stomberg, Margareta
    et al.
    University of Skövde, School of Life Sciences.
    Wickström, Kerstin
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Joelsson, Håkan
    University of Skövde, School of Life Sciences. Skaraborgs Hospital, Skövde, Sweden.
    Sjöström, Björn
    University of Skövde, School of Life Sciences. Sahlgrenska University Hospital, Göteborg, Sweden.
    Haljamäe, Hengo
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Postoperative pain management on surgical wards: do quality assurance strategies result in long-term effects on staff member attitudes and clinical outcomes?2003In: Pain Management Nursing, ISSN 1524-9042, E-ISSN 1532-8635, Vol. 4, no 1, p. 11-22Article in journal (Refereed)
    Abstract [en]

    Postoperative pain management (POPM) remains suboptimal on surgical wards in many countries despite the availability of effective analgesics, new technologies for drug administration, and clinical practice guidelines for pain management. The aim of the present study was to assess remaining long-term effects on pain management routines, patient experiences, and staff member attitudes in surgical wards more than 3 years after introduction of a quality assurance program for POPM and compare the findings to those of an organization where a corresponding systematic, entire hospital, quality assurance program had not been completed. A descriptive and comparative design, based on survey data from both patients (N = 110) and staff members (N = 51) on urologic surgery wards, was used. Significant (p < .05 to p < .0002) overall relationships were observed for identified shortages in pain management routines (lack of preoperative information, inadequate preoperative discussions on pain management, wait for pain killer) and reported experience of pain, nausea, or vomiting in the postoperative period. The quality assurance program, anesthesia-based pain services using a nurse-based anesthesiologist-supervised model, resulted in more adequate pain management routines, better patient satisfaction with POPM, and increased confidence in pain management among nurses on the surgical wards. On the basis of the present study it may be concluded that more than 3 years after the introduction of a quality assurance program for POPM in surgical wards, the pain management routines, patient experiences, and staff member attitudes have remained markedly improved and in accordance with the aims of accepted clinical practice guidelines for surgical pain management.

1 - 32 of 32
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