Relationship between bone mineral density and insulin resistance in polycystic ovary syndrome.
ABSTRACT The aim of the present study was to evaluate whether there is a relationship between bone mineral density (BMD) and insulin resistance and hyperinsulinemia in women with polycystic ovary syndrome (PCOS). The study consisted of 28 amenorrheic women with PCOS and 11 amenorrheic women without PCOS. Fifteen healthy women with normal ovulatory function, matched for age and body mass index (BMI), served as controls. BMD was measured at the lumbar spine and left femoral neck with dual-energy X-ray absorptiometry. Blood samples were obtained to measure serum levels of insulin, follicle-stimulating hormone, luteinizing hormone, sex hormone-binding globulin (SHBG), total and free testosterone, androstenedione and estradiol by radioimmunassay. Insulin resistance was estimated by the in sulin tolerance test (ITT), and K(ITT) was taken as the insulin sensitivity index. In the PCOS group, K(ITT) was significantly lower and insulin levels were higher than in either of the control groups (P < 0.001). BMD in the PCOS group was lower than in the healthy group and higher than in the amenorrheic control group (P < 0.05). In the PCOS group, there were positive correlations of BMD of the lumbar spine with insulin (r = 0.42: P < 0.05) and negative correlations of BMD with K(ITT) (r = -0.58; P < 0.001) and SHBG (r = -0.38; P < 0.05). The inverse association of BMD and K(ITT) was independent of BMI, insulin, SHBG, androstenedione, and free testosterone. In conclusion, insulin resistance and hyperinsulinemia in women with PCOS may be a relative protective factor against bone mineral loss.
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ABSTRACT: PCOS is a complex disorder and various features of this disorder may have great importance for bone metabolism. The aim of the study was to determine the relationship between existing hormonal disorders, and bone mineral density (BMD) in young women with PCOS.Journal of endocrinological investigation 09/2014; DOI:10.1007/s40618-014-0175-5 · 1.65 Impact Factor
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ABSTRACT: Polycystic ovarian syndrome (PCOS), the most common female endocrine disorder of unknown etiology, is characterized by reproductive abnormalities and associated metabolic conditions comprising insulin resistance, type 2 diabetes mellitus, and dyslipidemia. We previously reported that transgenic overexpression of nerve growth factor (NGF), a marker of sympathetic hyperactivity, directed to the ovary by the mouse 17α-hydroxylase/C17-20 lyase promoter (17NF) mice, results in ovarian abnormalities similar to those seen in PCOS women. To investigate whether ovarian overproduction of NGF also induces common metabolic alterations of PCOS, we assessed glucose homeostasis by glucose tolerance test, plasma insulin levels, and body composition by dual-energy x-ray absorptiometry scan in young female 17NF mice and wild-type mice. 17NF mice exhibited increased body weight and alterations in body fat distribution with a greater accumulation of visceral fat compared with sc fat (P < .01). 17NF mice also displayed glucose intolerance (P < .01), decreased insulin-mediated glucose disposal (P < .01), and hyperinsulinemia (P < .05), which, similar to PCOS patients, occurred independently of body weight. Additionally, 17NF mice exhibited increased sympathetic outflow observed as increased 24 hours of interscapular brown adipose tissue temperature. This change was evident during the dark period (7 pm to 7 am) and occurred concomitant with increased interscapular brown adipose tissue uncoupling protein 1 expression. These findings suggest that overexpression of NGF in the ovary may suffice to cause both reproductive and metabolic alterations characteristic of PCOS and support the hypothesis that sympathetic hyperactivity may contribute to the development and/or progression of PCOS.Endocrinology 09/2014; 155(11):en20141368. DOI:10.1210/en.2014-1368 · 4.72 Impact Factor