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To evaluate the effect of menopause and estrogen replacement therapy on leptin levels, 17 white postmenopausal women were recruited for the study. After an overnight fasting, blood samples were collected for LH, FSH, estradiol, testosterone, androstenedione, DHEA sulfate, insulin and leptin assays. Body mass index (BMI) and the waist-to-hip ratio were also evaluated. Patients were reanalyzed after a 12-week administration of transdermal estrogen patches delivering 50 microg 17beta-estradiol. The results were compared to those obtained from a group of 11 female volunteers in reproductive age, in whom basal blood was sampled during the early follicular phase of their cycle. Patients were divided into lean and obese according to their BMI. Obese postmenopausal women showed lower leptin levels when compared to premenopausal counterparts (25.1 +/- 5.9 vs. 37 +/- 11.3; p < 0.05), whereas no significant differences were found between the lean groups (14.5 +/- 3.8 vs. 14.4 +/- 4.9). Estrogen administration did not significantly change serum leptin concentrations in hypoestrogenized women (obese: 25.1 +/- 5.9 vs. 28. 6 +/- 9.2; lean: 14.4 +/- 4.9 vs. 17.6 +/- 7.2). A positive linear correlation was found between leptin plasma levels and BMI only in obese patients (r = 0.58; p < 0.01) both before and after estrogen treatment. Menopause is characterized by a decreased expression of the obese gene, even if estrogens do not seem to represent a main causal factor., (Copyright 2000 S. Karger AG, Basel)

The relationship between insulinaemia and obesity and glucose tolerance and the impact of pregnancy as risk factor for carbohydrate abnormalities were investigated in 91 consecutive patients with polycystic ovary syndrome (PCOS) aged 26-32 years. Fifteen normoglycaemic patients became pregnant within 6 months of the pregestational study using pharmacological induction of ovulation. Plasma concentrations of insulin and glucose after an oral glucose tolerance test (OGTT) were determined by immunoradiometric assay and glucose oxidase technique respectively. OGTT patients were classified according to their response as normoinsulinaemic (n = 46) or hyperinsulinaemic (n = 45). Impairment of glucose metabolism occurred in 12.1% (n = 11, 10 obese and one lean) of all PCOS subjects. Based on insulin secretion, 6.5% of normoinsulinaemic and 13.3% of hyperinsulinaemic patients had an impaired glucose tolerance and 2.3 and 2.2% respectively a non-insulin-dependent diabetes mellitus. Obese patients had higher values for area under the curve for insulin response to OGTT (I-AUC values) than lean patients, and the percentage above ideal body weight was greater in hyperinsulinaemic than in normoinsulinaemic patients. All hyperinsulinaemic (7/15) subjects who became pregnant developed an impairment of glucose metabolism during pregnancy. It is concluded that the PCOS population was at higher risk of developing carbohydrate abnormalities than the normal population of a similar reproductive age. Furthermore, those with abnormal insulin secretion at the pregestational stage may, during pregnancy, develop an impaired gestational glucose tolerance or gestational diabetes. [ABSTRACT FROM AUTHOR]

The relationship between insulinaemia and obesity and glucose tolerance and the impact of pregnancy as risk factor for carbohydrate abnormalities were investigated in 91 consecutive patients with polycystic ovary syndrome (PCOS) aged 26–32 years. Fifteen normoglycaemic patients became pregnant within 6 months of the pregestational study using pharmacological induction of ovulation. Plasma concentrations of insulin and glucose after an oral glucose tolerance test (OGTT) were determined by immunoradiometric assay and glucose oxidase technique respectively. OGTT patients were classified according to their response as normoinsulinaemic (n = 46) or hyperinsulinaemic (n = 45). Impairment of glucose metabolism occurred in 12.1% (n = 11, 10 obese and one lean) of all PCOS subjects. Based on insulin secretion, 6.5% of normoinsulinaemic and 133% of hyperinsulinaemic patients had an impaired glucose tolerance and 23 and 2.2% respectively a noninsulin-dependent diabetes mellitus. Obese patients had higher values for area under the curve for insulin response to OGTT (I-AUC values) than lean patients, and the percentage above ideal body weight was greater in hyperinsulinaemic than in normoinsulinaemic patients. All hyperinsulinaemic (7/15) subjects who became pregnant developed an impairment of glucose metabolism during pregnancy. It is concluded that the PCOS population was at higher risk of developing carbohydrate abnormalities than the normal population of a similar reproductive age. Furthermore, those with abnormal insulin secretion at the pregestational stage may, during pregnancy, develop an impaired gestational glucose tolerance or gestational diabetes. [ABSTRACT FROM PUBLISHER]