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  • 1.
    Stener-Victorin, Elisabet
    et al.
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Eriksson, Gustaw
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Shrestha, Man Mohan
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Rodriguez Paris, Valentina
    School of Biomedical Sciences, University of New South Wales, Sydney, Australia.
    Lu, Haojiang
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Banks, Jasmine
    School of Biomedical Sciences, University of New South Wales, Sydney, Australia ; Victor Chang Cardiac Research Institute, Darlinghurst, Sydney, NSW, Australia.
    Samad, Manisha
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Perian, Charlène
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Jude, Baptiste
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Engman, Viktor
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Boi, Roberto
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Nilsson, Emma
    Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Malmö, Sweden.
    Ling, Charlotte
    Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Malmö, Sweden.
    Nyström, Jenny
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Wernstedt Asterholm, Ingrid
    Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Turner, Nigel
    School of Biomedical Sciences, University of New South Wales, Sydney, Australia ; Victor Chang Cardiac Research Institute, Darlinghurst, Sydney, NSW, Australia.
    Lanner, Johanna T.
    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). Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Proteomic analysis shows decreased Type I fibers and ectopic fat accumulation in skeletal muscle from women with PCOS2024In: eLife, ISSN 2050-084X, Vol. 12Article in journal (Refereed)
    Abstract [en]

    Background: Polycystic ovary syndrome’s (PCOS) main feature is hyperandrogenism, which is linked to a higher risk of metabolic disorders in women. Gene expression analyses in adipose tissue and skeletal muscle reveal dysregulated metabolic pathways in women with PCOS, but these differences do not necessarily lead tochanges in protein levels and biological function. Methods: To advance our understanding of the molecular alterations in PCOS, we performed global proteomic and phosphorylation site analysis using tandem mass spectrometry. Adipose tissue and skeletal muscle were collected at baseline from 10 women with and without PCOS, and in women with PCOS after 5 weeks of treatment with electrical stimulation. Results: Perilipin-1, a protein that typically coats the surface of lipid droplets in adipocytes, was increased whereas proteins involved in muscle contraction and type I muscle fiber function were downregulated in PCOS muscle. Proteins in the thick and thin filaments had many altered phosphorylation sites, indicating differences in protein activity and function. The upregulated proteins in muscle post treatment were enriched in pathways involved in extracellular matrix organization and wound healing, which may reflect a protective adaptation to repeated contractions and tissue damage due to needling. A similar, albeit less pronounced, upregulation in extracellular matrix organization pathways was also seen in adipose tissue. Conclusions: Our results suggest that hyperandrogenic women with PCOS have higher levels of extramyocellular lipids and fewer oxidative insulin-sensitive type I muscle fibers. These could be key factors leading insulin resistance in PCOS muscle while electric stimulation-induced tissue remodeling may be protective.

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