Gestational diabetes mellitus (GDM) and polycystic ovary syndrome (PCOS) are distinct pathologies with impaired insulin sensitivity as a common feature. The aim of this study was to evaluate the response of fat tissue adipokines and gastrointestinal incretins to glucose load in patients diagnosed with one of the two disorders and to compare it with healthy controls. Oral glucose tolerance test (oGTT) was performed in 77 lean young women: 22 had positive history of GDM, 19 were PCOS patients, and 36 were healthy controls. Hormones were evaluated in fasting and in 60 min intervals during the 3 h oGTT using Bio-Plex ProHuman Diabetes 10-Plex Assay for C-peptide, ghrelin, GIP, GLP1, glucagon, insulin, leptin, total PAI1, resistin, visfatin and Bio-Plex ProHuman Diabetes Adipsin and Adiponectin Assays (Bio-Rad). Despite lean body composition, both PCOS and GDM women were more insulin resistant than controls. Significant postchallenge differences between the GDM and PCOS groups were observed in secretion of adipsin, leptin, glucagon, visfatin, ghrelin, GIP, and also GLP1 with higher levels in GDM. Conversely, PCOS was associated with the highest resistin, C-peptide, and PAI1 levels. Our data suggest that decreased insulin sensitivity observed in lean women with GDM and PCOS is associated with distinct hormonal response of fat and gastrointestinal tissue to glucose load., D. Vejrazkova, O. Lischkova, M. Vankova, S. Stanicka, J. Vrbikova, P. Lukasova, J. Vcelak, G. Vacinova, B. Bendlova., and Obsahuje bibliografii
Objective: To examine the impact of family history of diabetes mellitus 2 (DM 2) on insulin sensitivity and secretion in lean women with polycystic ovary syndrome (PCOS). Thirteen healthy women (C), 14 PCOS without family history of DM 2 (FH-) and 8 PCOS with family history of DM 2 (FH+) were examined using euglycemic hyperinsulinemic clamp and an arginine secretion test (insulin and glucagon at fasting glycemia (AIRFG and AGRFG) and at hyperglycemia (AIR14 and AG 14)). FH+ women were more insulin resistant than FH- with lower insulin sensitivity index corrected per lean body mass (p<0.05). They had significantly higher triglycerides (p<0.05) and lower HDL-cholesterol (p<0.05) than C or FH- women. Concerning insulin secretion, AIR FG was increased in FH+ women comparing FH- women (p<0.05). Disposition indices derived from AIRFG or AIR14 and insulin sensitivity index did not differ between FH+ or FH-. Thus, women with PCOS with the concomitant family history of DM 2 have lower insulin sensitivity than healthy control women. Insulin resistance observed in these women with PCOS is compensated by increased insulin secretion., J. Vrbíková, T. Grimmichová, K, Dvořáková, M. Hill, S. Stanická, K. Vondra., and Obsahuje bibliografii a bibliografické odkazy
The aim of our study was to evaluate rapid insulin pulses and insulin secretion regularity in fasting state in lean women with polycystic ovary syndrome (PCOS) in comparison to lean healthy women. PCOS (n=8) and controls (n=7) underwent every minute blood sampling for 60 min. Insulin pulsatility was assessed by deconvolution and insulin secretion regularity by approximate entropy methodology. PCOS had higher testosterone (p<0.02), prolactin (p<0.05) and lower sex hormone binding globulin (SHBG) (p<0.0006) levels than controls. Approximate entropy, insulin pulse frequency, mass, amplitude and interpulse interval did not differ between PCOS and controls. PCOS had broader insulin peaks determined by a common half-duration (p<0.07). Burst mass correlated positively with testosterone (p<0.05) and negatively with SHBG (p<0.0004) and common half-duration correlated positively with prolactin (p<0.008) and cortisol levels (p<0.03). Approximate entropy positively correlated with BMI (p<0.04) and prolactin (p<0.03). Lean PCOS patients tended to have broader insulin peaks in comparison to healthy controls. Prolactin, androgens and cortisol might participate in alteration of insulin secretion in PCOS-affected women. Body weight and prolactin levels could influence insulin secretion regularity., T. Grimmichová, J. Vrbíková, P. Matucha, K. Vondra, P. P. Veldhuis, M. L. Johnson., and Obsahuje bibliografii a bibliografické odkazy
Numerous hypotheses have been proposed about the pathogenesis of the polycystic ovarian syndrome (PCOS). However, hormonal control of persistent follicles has not be enestablished. The objective of the present study was to compare the follicular structure and hormonal profiles of rats treated with the adrenocor ticotrophic hormone (ACTH) with two experimental models of PCOS. ACTH-treated animals were compared with those exposed to continuous light, those treated with estradiol valerate, and with control (in proestrous and diestrous). Serum hormone levels, histomorphometrical changes, and immunoexpression of vimentin, cytokeratins, cadherins, and proliferating cell nuclear antigen (PCNA) were examined. Treatment with ACTH resulted in an elevation of corticosterone secretion with LH reduction but without changes in ovarian morphology. Although stress (or ACTH) stimulation may be only one of pathophysiological mechanisms involved in follicular cystathogenesis in other species, we do not have important evidence to suppose that this would happen in rats., C. Bavaralle, N. R. Salvetti, G. A. Mira, J. A. Lorente, H. H. Ortega., and Obsahuje bibliografii a bibliografické odkazy