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inhibition of the insulin-mediated phosphorylation of CCAAT/enhancer-binding protein-β (C/EBPβ) prevents adipocyte differentiation in vitro . Yoo et al. ( 14 ) studied the correlation of GPC4 levels with body-fat distribution, insulin resistance
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implicated in various physiological processes such as insulin sensitivity, adipocyte differentiation, and vascular function, and has been shown to regulate the formation and function of MAMs ( 16 ). Taken together, mitochondria ( 17 ) and ER ( 18 ) play
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that the effect of increased BMI on IR is proportionally more evident in PCOS women than in controls ( 46 ). This could possibly be due to the presence of dysfunctional adipocytes and/or a preferential visceral distribution of fat in PCOS ( 46 , 47
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hypertrophy of adipocyte cells both in subcutaneous and visceral adipose tissue, as well as increased inflammation and fibrosis, compared with premenopausal women ( 9 ). One mechanism for the postmenopausal body fat redistribution may be the upregulation of
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subcutaneous adipose tissue differs in women with polycystic ovary syndrome and controls matched pair-wise for age, body weight, and body mass index . Adipocyte 2014 3 190 – 196 . ( https://doi.org/10.4161/adip.28731 ) 48 Ragy MM Abdel-Hamid HA & Toni