Relationship among plasma adipokines, insulin and androgens level as well as biochemical glycemic and lipidemic markers with incidence of PCOS in women with normal BMI.
ABSTRACT Polycystic ovary syndrome (PCOS) is an endocrine disorder in women. Omentin-1 and vaspin are secretary adipokines that are produced by the visceral adipose tissue. These levels change in obese women with PCOS. The aim of this study is to investigate whether omentin and vaspin levels change in nonobese PCOS subjects. This study is a cross-sectional case control study in which 39 women with PCOS were picked out for this study. The inclusion criteria were based on the Rotterdam 2003 diagnostic criteria. The control group consisted of 39 women with normal pelvic sonographic reports having regular menstruation and showing no signs of infertility. The fasting plasma glucose (FPG), triglyceride (TG), Chol, and high-density lipoprotein cholesterol (HDL-C), insulin, testosterone, omentin and vaspin were measured by the enzymatic methods. The differences within these groups were calculated by the un-paired t-test and the Mann-Whitney test. The results from this study show a significant increase in the amount of insulin, testosterone, homeostasis model assessments for insulin resistance, TG and lower HDL in the patient group. No significant differences were seen in omentin, vaspin, FPG, Cho, low-density lipoprotein, very low-density lipoprotein cholesterol, blood urea nitrogen, Cr and homeostasis model assessments for B cell function levels between groups. Results show that PCOS is not a determinant of decreased omentin and vaspin plasma levels and those high androgen level and insulin resistances are warning signs of PCOS.
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ABSTRACT: It is now clear that PCOS is often associated with profound insulin resistance as well as with defects in insulin secretion. These abnormalities, together with obesity, explain the substantially increased prevalence of glucose intolerance in PCOS. Moreover, since PCOS is an extremely common disorder, PCOS-related insulin resistance is an important cause of NIDDM in women (Table 3). The insulin resistance in at least 50% of PCOS women appears to be related to excessive serine phosphorylation of the insulin receptor. A factor extrinsic to the insulin receptor, presumably a serine/threonine kinase, causes this abnormality and is an example of an important new mechanism for human insulin resistance related to factors controlling insulin receptor signaling. Serine phosphorylation appears to modulate the activity of the key regulatory enzyme of androgen biosynthesis, P450c17. It is thus possible that a single defect produces both the insulin resistance and the hyperandrogenism in some PCOS women (Fig. 19). Recent studies strongly suggest that insulin is acting through its own receptor (rather than the IGF-I receptor) in PCOS to augment not only ovarian and adrenal steroidogenesis but also pituitary LH release. Indeed, the defect in insulin action appears to be selective, affecting glucose metabolism but not cell growth. Since PCOS usually has a menarchal age of onset, this makes it a particularly appropriate disorder in which to examine the ontogeny of defects in carbohydrate metabolism and for ascertaining large three-generation kindreds for positional cloning studies to identify NIDDM genes. Although the presence of lipid abnormalities, dysfibrinolysis, and insulin resistance would be predicted to place PCOS women at high risk for cardiovascular disease, appropriate prospective studies are necessary to directly assess this.Endocrine Reviews 01/1998; 18(6):774-800. · 19.36 Impact Factor
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ABSTRACT: Functional ovarian hyperandrogenism, a variant of polycystic ovary syndrome, is often associated with hyperinsulinism and dyslipidemia. The mechanisms interlinking this triad are poorly understood; both hyperandrogenism and hyperinsulinism have been proposed as factors involved in the pathogenesis of the dyslipidemia. Precocious pubarche (PP) in girls is a risk factor for subsequent anovulation, ovarian and adrenal hyperandrogenism, hyperinsulinism and dyslipidemia. Flutamide, a nonsteroidal antiandrogen, is known to be effective in reducing hirsutism in patients with ovarian hyperandrogenism. However, the effects of flutamide on the endocrine-metabolic correlates of hyperandrogenism are uncertain. We assessed the effects of low dose flutamide treatment (250 mg daily for 18 months) on hormonal and metabolic variables in 18 nonobese adolescent girls (age, 16.8 +/- 0.3 yr) with functional ovarian hyperandrogenism (diagnosis by GnRH agonist test) after PP. Flutamide treatment was accompanied by a marked decrease in the hirsutism score, free androgen index, and testosterone, androstenedione, and dehydroepiandrosterone levels and by an increase in sex hormone-binding globulin concentrations. However, there were no substantial changes in the pattern of menstrual cycles, gonadotropin, estradiol, or dehydroepiandrosterone sulfate concentrations, and there was no detectable effect on the 17-hydroxyprogesterone response to GnRH agonist. Serum triglycerides, total cholesterol, and low-density lipoprotein cholesterol levels decreased markedly during flutamide therapy, whereas high-density lipoprotein cholesterol, fasting glycemia/insulinemia, and the insulin response to a glucose load remained unchanged. Flutamide was well tolerated. In conclusion, low dose flutamide treatment was found to be an effective and safe approach to reduce hirsutism and circulating androgen, low-density lipoprotein cholesterol, and triglyceride levels in girls with functional ovarian hyperandrogenism after PP. However, flutamide failed to increase high-density lipoprotein cholesterol levels or decrease hyperinsulinemia, i.e. to affect two major risk factors for subsequent cardiovascular disease.Journal of Clinical Endocrinology & Metabolism 10/2000; 85(9):3251-5. · 6.31 Impact Factor
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ABSTRACT: Omentin-1 is a novel adipokine that increases insulin sensitivity and is expressed in visceral adipose tissue. The aim of this study was to determine the metabolic parameters that influence plasma omentin-1 levels in women with polycystic ovary syndrome (PCOS). A cross-sectional study was performed in 87 women with PCOS and 53 body mass index (BMI)-matched healthy controls including 39 non-obese, normal-weight (NW) PCOS women with normal glucose tolerance (NGT) and 44 BMI- and homeostasis model assessment (HOMA)-matched controls. Indices of insulin sensitivity, metabolic variables, circulating androgen levels, serum adiponectin, and omentin-1 levels were measured. A 75 g oral glucose tolerance test was performed in all participants. Plasma omentin-1 levels were significantly lower in women with PCOS compared with those in BMI-matched controls (P<0.001). A significantly lower level of plasma omentin-1 was observed in non-obese women with PCOS and NGT compared with that in BMI- and HOMA-matched controls (P<0.001). Omentin-1 level was negatively correlated with BMI, indices of insulin sensitivity, and circulating androgens and was associated with greater 2 h postprandial glucose, C-peptide, and insulin levels compared with fasting values. Within the NW and NGT groups, omentin-1 levels remained negatively correlated with BMI, 2 h postprandial C-peptide, and circulating androgens and demonstrated a negative linear trend according to quartile of free testosterone (P=0.028). Plasma levels of omentin-1 were reduced in non-obese women with PCOS and NGT. Postprandial hyperinsulinemia and hyperglycemia contributed more to lower omentin-1 levels than did fasting values in the setting of PCOS. Increased androgen levels contributed to decreased omentin-1 levels in women with PCOS.European Journal of Endocrinology 08/2011; 165(5):789-96. · 3.69 Impact Factor