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  • 1.
    Bauzá-Thorbrügge, Marco
    et al.
    Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Vujičić, Milica
    Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Chanclón, Belén
    Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Palsdottir, Vilborg
    Unit for Endocrine Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Pillon, Nicolas J.
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Benrick, Anna
    University of Skövde, School of Health Sciences. University of Skövde, Digital Health Research (DHEAR). Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Wernstedt Asterholm, Ingrid
    Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
    Adiponectin stimulates Sca1+CD34-adipocyte precursor cells associated with hyperplastic expansion and beiging of brown and white adipose tissue2024In: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 151, article id 155716Article in journal (Refereed)
    Abstract [en]

    Background: The adipocyte hormone adiponectin improves insulin sensitivity and there is an inverse correlation between adiponectin levels and type-2 diabetes risk. Previous research shows that adiponectin remodels the adipose tissue into a more efficient metabolic sink. For instance, mice that overexpress adiponectin show increased capacity for hyperplastic adipose tissue expansion as evident from smaller and metabolically more active white adipocytes. In contrast, the brown adipose tissue (BAT) of these mice looks “whiter” possibly indicating reduced metabolic activity. Here, we aimed to further establish the effect of adiponectin on adipose tissue expansion and adipocyte mitochondrial function as well as to unravel mechanistic aspects in this area. Methods: Brown and white adipose tissues from adiponectin overexpressing (APN tg) mice and littermate wildtype controls, housed at room and cold temperature, were studied by histological, gene/protein expression and flow cytometry analyses. Metabolic and mitochondrial functions were studied by radiotracers and Seahorse-based technology. In addition, mitochondrial function was assessed in cultured adiponectin deficient adipocytes from APN knockout and heterozygote mice. Results: APN tg BAT displayed increased proliferation prenatally leading to enlarged BAT. Postnatally, APN tg BAT turned whiter than control BAT, confirming previous reports. Furthermore, elevated adiponectin augmented the sympathetic innervation/activation within adipose tissue. APN tg BAT displayed reduced metabolic activity and reduced mitochondrial oxygen consumption rate (OCR). In contrast, APN tg inguinal white adipose tissue (IWAT) displayed enhanced metabolic activity. These metabolic differences between genotypes were apparent also in cultured adipocytes differentiated from BAT and IWAT stroma vascular fraction, and the OCR was reduced in both brown and white APN heterozygote adipocytes. In both APN tg BAT and IWAT, the mesenchymal stem cell-related genes were upregulated along with an increased abundance of Lineage−Sca1+CD34− “beige-like” adipocyte precursor cells. In vitro, the adiponectin receptor agonist Adiporon increased the expression of the proliferation marker Pcna and decreased the expression of Cd34 in Sca1+ mesenchymal stem cells. Conclusions: We propose that the seemingly opposite effect of adiponectin on BAT and IWAT is mediated by a common mechanism; while reduced adiponectin levels are linked to lower adipocyte OCR, elevated adiponectin levels stimulate expansion of adipocyte precursor cells that produce adipocytes with intrinsically higher metabolic rate than classical white but lower metabolic rate than classical brown adipocytes. Moreover, adiponectin can modify the adipocytes' metabolic activity directly and by enhancing the sympathetic innervation within a fat depot. 

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  • 2.
    Sjöberg, Sara
    et al.
    Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
    Fogelstrand, Linda
    Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
    Hulthe, Johannes
    Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
    Fagerberg, Björn
    Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
    Krettek, Alexandra
    Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden / Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, Göteborg, Sweden.
    Circulating soluble CD44 is higher among women than men and is not associated with cardiovascular risk factors or subclinical atherosclerosis2005In: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 54, no 2, p. 139-141Article in journal (Refereed)
    Abstract [en]

    In the present study, the associations between the plasma concentration of soluble CD44 (sCD44), sex, cardiovascular risk factors, and ultrasound-assessed measures of carotid atherosclerosis were examined in 2 groups of 61- and 64-year-old men and women from population-based samples. Women had higher levels of circulating sCD44 than men. There were no associations between sCD44 and cardiovascular risk factors or subclinical atherosclerosis.

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