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Effects of metformin on insulin secretion, insulin action, and ovarian steroidogenesis in women with polycystic ovary syndrome

It is concluded that hyperinsulinemia and androgen excess in obese nondiabetic women with PCOS are not improved by the administration of metformin.
Hyperinsulinemia contributes to the ovarian androgen overproduction and glucose intolerance of polycystic ovary syndrome (PCOS). We sought to determine whether metformin would reduce insulin levels in obese, nondiabetic women with PCOS during a period of weight maintenance and thus attenuate the ovarian steroidogenic response to the GnRH agonist leuprolide. All subjects (n = 14) had an oral glucose tolerance test, a GnRH agonist (leuprolide) test, a frequently sampled iv glucose tolerance test, graded and oscillatory glucose infusions, and a dual energy x-ray absorptiometry scan before and after treatment with metformin (850 mg, orally, three times daily for 12 weeks). With weight maintenance (body mass index: pretreatment, 39.0 +/- 7.7 kg/m2, posttreatment, 39.1 +/- 7.9 kg/m2), oral glucose tolerance, insulin sensitivity (Si; 0.87 +/- 0.82 vs. 0.74 +/- 0.63 x 10(-5) min-1/ pmol.L), and the relationship between Si and first phase insulin secretion (AIRg vs. Si) were not improved by metformin. The insulin secretory response to glucose, administered in both graded and oscillatory fashions, was likewise unaltered in response to metformin. Free testosterone levels remained about 2-fold elevated (pretreatment, 26.6 +/- 12.7 pg/mL; posttreatment, 22.4 +/- 9.8 pg/mL). Both basal and stimulated LH and FSH levels were unaffected by metformin. The mean responses to leuprolide of 17-hydroxyprogesterone (pretreatment, 387 +/- 158 ng/dL; posttreatment, 329 +/- 116 ng/dL) as well as those of the other ovarian secretory products (androstenedione, dehydroepiandrosterone, progesterone, and estradiol) were not attenuated by metformin. We conclude that hyperinsulinemia and androgen excess in obese nondiabetic women with PCOS are not improved by the administration of metformin.

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Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis.

TL;DR: 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.
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Polycystic ovary syndrome.

TL;DR: PCOS can impact women’s reproductive health, leading to anovulatory infertility and higher rate of early pregnancy loss, and the risks of diabetes, cardiovascular disease, hypertension, metabolic syndrome, and endometrial cancer among PCOS patients are significantly increased.

Polycystic Ovary Syndrome

TL;DR: It is of interest to realize that polycystic ovary syndrome has moved from a histology diagnosis of ovarian tissue to a heterogeneous clinical syndrome, to a reproductive endocrine abnormality with elevated serum luteinizing hormone and androgen levels, and to a metabolic disease characterized by hyperinsulinemia and dyslipidemia.
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The insulin-related ovarian regulatory system in health and disease.

TL;DR: The Insulin-Related Ovarian Regulatory System: Implications for Therapy and Therapeutic use are summarized.
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Obesity and the polycystic ovary syndrome

TL;DR: Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCos women.
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Spectral analysis and its applications

TL;DR: In this paper, Spectral Analysis and its Applications, the authors present a set of applications of spectral analysis and its application in the field of spectroscopy, including the following:
Journal ArticleDOI

Immunoassay of Insulin: Two Antibody System: Plasma Insulin Levels of Normal, Subdiabetic and Diabetic Rats

Carl R Morgan, +1 more
- 01 Mar 1963 - 
TL;DR: A two antibody system of insulin assay for immunoassay of insulin induces the production of specific nonprecipitating antibodies, both in experimental animals and in humans.
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Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose.

TL;DR: The feasibility of the minimal model technique to determine the etiology of impaired glucose tolerance is demonstrated and it is demonstrated that subjects (regardless of weight) could be segregated into good and lower tolerance by the product of second-phase beta-cell responsivity and insulin sensitivity.
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Dual-energy x-ray absorptiometry for total-body and regional bone-mineral and soft-tissue composition.

TL;DR: Bone mineral density (BMD) and soft-tissue composition of the total body and major subregions were measured with dual-energy x-ray absorptiometry (DEXA) and there were no significant differences in mean results or in precision errors between the two speeds.
Journal ArticleDOI

Quantification of the relationship between insulin sensitivity and beta-cell function in human subjects. Evidence for a hyperbolic function.

TL;DR: In human subjects with normal glucose tolerance and varying degrees of obesity, β-cell function varies quantitatively with differences in insulin sensitivity, consistent with a regulated feedback loop control system.
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