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considered potential causes ( 6 ). However, increasing evidence ( 7 ) shows that insulin resistance and compensatory hyperinsulinemia play an important role in the pathogenesis of PCOS. The progression of insulin resistance as well as the regulation of
Department of Medical and Surgical Sciences (DIMEC), Alma Mater Studiorum University of Bologna, Bologna, Italy
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obese PCOS women, visceral adiposity, insulin resistance (IR), and compensatory hyperinsulinemia are usually the triggering pathogenetic factors, whereas androgen excess is frequently mild and sometimes secondary to visceral obesity and IR ( 2
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International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Section of Biostatistics, University of Copenhagen, Copenhagen, Denmark
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International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Fertility, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
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Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
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well as an increased risk of developing insulin resistance, metabolic syndrome, and osteoporosis ( 1 ). Low to low-normal serum concentrations of testosterone are seen in most adults with KS, but nearly all have highly elevated concentrations of
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relation between PCOS and BD is less well-known. PCOS is associated with central obesity, dyslipidemia, hypertension, and insulin resistance ( 7 ), which all have been described to decrease BD ( 8 , 9 , 10 , 11 ). However, hyperandrogenism, one of the
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, which are widely accepted contributors to insulin resistance ( 3 ). The hypogonadal pathology assumption remains challenged, given cardiometabolic disease risk factors are identified in younger cohorts of boys with KS naïve to years of hypogonadism, as
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LH, estradiol (E2), follicle-stimulating hormone (FSH) and insulin were tested using a chemiluminescence immunometric assay (Mindray, CL-2000i, Shenzhen, China). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as insulin
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-C), LDL-cholesterol (LDL-C), total cholesterol (TC), triglycerides (TG), apolipoprotein (apo) A1, and apoB levels, plasma Glu and insulin (Ins) concentrations, and the homeostatic model assessment of insulin resistance (HOMA-IR) were determined or
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Department of Endocrinology and Diabetes, The First Affiliated Hospital, Xiamen University, Xiamen, China
Fujian Province Key Laboratory of Diabetes Translational Medicine, Xiamen, China
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obesity, and the phenomenon was also seen in another study ( 15 ). The link between AMH and central obesity may be related to the following factors. First of all, central or abdominal obesity is associated with greater insulin resistance (IR) likely
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ovaries on ultrasound ( 1 , 2 ). It affects 4–21% of women worldwide depending on the region and nationality studied and the diagnostic criteria used ( 3 , 4 ). PCOS is associated with an increased risk of insulin resistance (IR), hyperinsulinemia, type
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, including abnormal follicular development, insulin resistance, and excess androgen production ( 2 ). Among these changes, abnormal follicular development and insulin resistance are more commonly observed. However, the pathogenesis and molecular regulatory