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Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study

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 overwei...

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Autores principales: Feichtinger, Michael, Linder, Tina, Rosicky, Ingo, Eppel, Daniel, Schatten, Christian, Eppel, Wolfgang, Husslein, Peter, Tura, Andrea, Göbl, Christian S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7795887/
https://www.ncbi.nlm.nih.gov/pubmed/33374430
http://dx.doi.org/10.3390/jcm10010035
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author Feichtinger, Michael
Linder, Tina
Rosicky, Ingo
Eppel, Daniel
Schatten, Christian
Eppel, Wolfgang
Husslein, Peter
Tura, Andrea
Göbl, Christian S.
author_facet Feichtinger, Michael
Linder, Tina
Rosicky, Ingo
Eppel, Daniel
Schatten, Christian
Eppel, Wolfgang
Husslein, Peter
Tura, Andrea
Göbl, Christian S.
author_sort Feichtinger, Michael
collection PubMed
description 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.
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spelling pubmed-77958872021-01-10 Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study Feichtinger, Michael Linder, Tina Rosicky, Ingo Eppel, Daniel Schatten, Christian Eppel, Wolfgang Husslein, Peter Tura, Andrea Göbl, Christian S. J Clin Med Article 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. MDPI 2020-12-24 /pmc/articles/PMC7795887/ /pubmed/33374430 http://dx.doi.org/10.3390/jcm10010035 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Feichtinger, Michael
Linder, Tina
Rosicky, Ingo
Eppel, Daniel
Schatten, Christian
Eppel, Wolfgang
Husslein, Peter
Tura, Andrea
Göbl, Christian S.
Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title_full Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title_fullStr Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title_full_unstemmed Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title_short Maternal Overweight vs. Polycystic Ovary Syndrome: Disentangling Their Impact on Insulin Action in Pregnancy—A Prospective Study
title_sort maternal overweight vs. polycystic ovary syndrome: disentangling their impact on insulin action in pregnancy—a prospective study
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7795887/
https://www.ncbi.nlm.nih.gov/pubmed/33374430
http://dx.doi.org/10.3390/jcm10010035
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