scholarly journals Preserved Insulin Sensitivity and β-Cell Activity, but Decreased Glucose Effectiveness in Normal-Weight Women with the Polycystic Ovary Syndrome

2005 ◽  
Vol 90 (6) ◽  
pp. 3381-3386 ◽  
Author(s):  
G. Gennarelli ◽  
V. Rovei ◽  
R. F. Novi ◽  
J. Holte ◽  
F. Bongioanni ◽  
...  
2014 ◽  
Vol 99 (11) ◽  
pp. E2244-E2251 ◽  
Author(s):  
Frank González ◽  
Chang Ling Sia ◽  
Marguerite K. Shepard ◽  
Neal S. Rote ◽  
Judi Minium

Context: Excess adipose tissue is a source of inflammation. Polycystic ovary syndrome (PCOS) is a proinflammatory state and is often associated with excess abdominal adiposity (AA) alone and/or frank obesity. Objective: To determine the effect of glucose ingestion on cytokine release from mononuclear cells (MNC) in women with PCOS with and without excess AA and/or obesity. Design: A cross-sectional study. Setting: Academic medical center. Patients: Twenty-three women with PCOS (seven normal weight with normal AA, eight normal weight with excess AA, eight obese) and 24 ovulatory controls (eight normal weight with normal AA, eight normal weight with excess AA, eight obese). Intervention: Three-hour 75-g oral glucose tolerance test (OGTT). Main Outcome Measures: Body composition was measured by dual energy x-ray absorptiometry. Insulin sensitivity was derived from the OGTT (ISOGTT). TNFα, IL-6, and IL-1β release was measured in supernatants of cultured MNC isolated from blood samples drawn while fasting and 2 hours after glucose ingestion. Results: Insulin sensitivity was lower in obese subjects regardless of PCOS status and in normal-weight women with PCOS compared with normal-weight controls regardless of body composition status. In response to glucose ingestion, MNC-derived TNFα, IL-6, and IL-1β release decreased in both normal-weight control groups but failed to suppress in either normal-weight PCOS group and in obese women regardless of PCOS status. For the combined groups, the cytokine responses were negatively correlated with insulin sensitivity and positively correlated with abdominal fat and androgens. Conclusions: Women with PCOS fail to suppress MNC-derived cytokine release in response to glucose ingestion, and this response is independent of excess adiposity. Nevertheless, a similar response is also a feature of obesity per se. Circulating MNC and excess adipose tissue are separate and distinct sources of inflammation in this population.


Author(s):  
Sebastião Freitas de Medeiros ◽  
Laura Camila Antunes Angelo ◽  
Matheus Antônio Souto de Medeiros ◽  
Bruna Barcelo Barbosa ◽  
Márcia Marly Winck Yamamoto

AbstractBackgroundHyperandrogenemic polycystic ovary syndrome (PCOS) may have occult corticosteroidogenic enzyme abnormalities. The current study compares the activities of 11β-hydroxylase between normoandrogenemic PCOS (NA-PCOS) and hyperandrogenemic PCOS (HA-PCOS) phenotypes.Materials and methodsAnthropometric, and biochemical variables were compared between normal cycling women [n = 272] and those with PCOS [n = 453]; either normoandrogenemic [n = 98] or hyperandrogenemic [n = 355]. Univariate and multivariate logistic regression analyses were performed using 11β-hydroxylase enzyme activity as the criterion variable.Results11β-Hydroxylase enzyme activity tended to be slightly higher in both PCOS subgroups and did not change with ethnicity. Using univariate logistic regression, 11β-hydroxylase activity in controls was associated with dehydroepiandrosterone, insulin, homeostatic model for insulin resistance (HOMA-IR), and high-density lipoprotein cholesterol (HDL-C). In NA-PCOS women the activity of 11β-hydroxylase was associated with estradiol (E2), androstenedione (A4), and androstenedione/dehydroepiandrosterone ratio; in the hyperandrogenemic (HA-PCOS) group, 11β-hydroxylase activity associated with sex-hormone binding globulin (SHBG), 17-hydroxypregnenolone (17-OHPE), fasting glucose, and β-cell activity. After multivariate logistic regression, androstenedione/dehydroepiandrosterone ratio, and β-cell activity were the best predictors of 11β-hydroxylase activity in controls; in NA-PCOS group only androstenedione/dehydroepiandrosterone ratio was confirmed as a significant predictor of 11β-hydroxylase activity, and in HA-PCOS patients, 17-OHPE and β-cell activity demonstrated to be significant predictors.Conclusions11β-Hydroxylase activity was equal in different ethnicities. The prevalence of decreased 11β-hydroxylase activity was higher in the HA-PCOS phenotype. 17-OHPE, and β-cell function are significant predictors of 11β-hydroxylase activity in HA-PCOS subjects. These findings may help to identify which PCOS patient would have benefit in measuring 11-deoxycortisol (compound S) and 11β-hydroxylase enzyme activity.


2020 ◽  
Vol 10 (1) ◽  
pp. 35
Author(s):  
Michael Feichtinger ◽  
Tina Linder ◽  
Ingo Rosicky ◽  
Daniel Eppel ◽  
Christian Schatten ◽  
...  

Background: To investigate insulin sensitivity and glucose metabolism in pregnant lean and overweight polycystic ovary syndrome (PCOS) patients vs. lean and overweight controls without PCOS. Methods: Prospective cohort study on 67 pregnant women (31 with PCOS and 36 controls, subdivided into overweight or obese and normal weight). All women underwent a 2h-OGTT including glucose, insulin, and C-peptide in early- and mid-gestation and were followed-up until delivery. Results: Insulin sensitivity and glucometabolic parameters were comparable between PCOS patients and controls, whereas marked differences were observed between overweight/obese and lean mothers. Impaired whole-body insulin sensitivity at early pregnancy is mainly a consequence of higher BMI (body mass index; p < 0.001) compared to PCOS (p = 0.216), whereby no interaction between overweight/obesity and PCOS was observed (p = 0.194). Moreover, overweight was significantly associated with gestational diabetes (p = 0.0003), whereas there were no differences between women with and without PCOS (p = 0.51). Birth weight was inversely related to whole-body insulin sensitivity (rho = −0.33, p = 0.014) and positively associated with higher pregestational BMI (rho = 0.33, p = 0.012), whereas there was no association with PCOS. Conclusions: Impaired insulin action was mainly a consequence of overweight rather than PCOS. Our data suggest that overweight is more relevant than PCOS for the effects on insulin sensitivity and impaired glucose metabolism.


2007 ◽  
Vol 23 (5) ◽  
pp. 273-278 ◽  
Author(s):  
José A. M. Marcondes ◽  
Sylvia A. Y. Yamashita ◽  
Gustavo A. R. Maciel ◽  
Edmund C. Baracat ◽  
Alfredo Halpern

1997 ◽  
Vol 11 (5) ◽  
pp. 315-320 ◽  
Author(s):  
D. Micić ◽  
Dj. Macut ◽  
V. Popović ◽  
M. Ŝumarac-Dumanović ◽  
A. Kendereŝki ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document