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Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus

Background: Gestational diabetes mellitus (GDM) is a pregnancy complication characterized by second trimester hyperglycemia. Untreated, GDM is related to an increased risk for adverse pregnancy outcomes. Both beta cell dysfunction and insulin resistance underlie impaired glucose tolerance. Understan...

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Autores principales: Ellerbrock, Jonas, Spaanderman, Benthe, van Drongelen, Joris, Mulder, Eva, Lopes van Balen, Veronica, Schiffer, Veronique, Jorissen, Laura, Alers, Robert-Jan, Leenen, Jeanine, Ghossein-Doha, Chahinda, Spaanderman, Marc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231208/
https://www.ncbi.nlm.nih.gov/pubmed/35745174
http://dx.doi.org/10.3390/nu14122444
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author Ellerbrock, Jonas
Spaanderman, Benthe
van Drongelen, Joris
Mulder, Eva
Lopes van Balen, Veronica
Schiffer, Veronique
Jorissen, Laura
Alers, Robert-Jan
Leenen, Jeanine
Ghossein-Doha, Chahinda
Spaanderman, Marc
author_facet Ellerbrock, Jonas
Spaanderman, Benthe
van Drongelen, Joris
Mulder, Eva
Lopes van Balen, Veronica
Schiffer, Veronique
Jorissen, Laura
Alers, Robert-Jan
Leenen, Jeanine
Ghossein-Doha, Chahinda
Spaanderman, Marc
author_sort Ellerbrock, Jonas
collection PubMed
description Background: Gestational diabetes mellitus (GDM) is a pregnancy complication characterized by second trimester hyperglycemia. Untreated, GDM is related to an increased risk for adverse pregnancy outcomes. Both beta cell dysfunction and insulin resistance underlie impaired glucose tolerance. Understanding the dominant mechanism predisposing to GDM may be important to provide effective treatment in order to improve perinatal outcomes. We hypothesize that insulin resistance rather that beta cell dysfunction predisposes to GDM. Methods: A 75g oral glucose tolerance test (OGTT) was performed on 2112 second-trimester pregnant women to determine the relationship between insulin resistance (HOMA-IR), beta cell function (HOMA-β), and the prevalence of abnormal glucose handling. Results: High insulin resistance raised the risk of GDM (relative risk (RR) 6.1, 95% confidence interval (CI) (4.4–8.5)), as did beta cell dysfunction (RR 3.8, 95% CI (2.7–5.4)). High insulin resistance, but not beta cell function, enhances the necessity for additional glucose lowering medication on top of a low carbohydrate diet in women diagnosed with GDM. Conclusions: Both high insulin resistance and beta cell dysfunction increase the risk of GDM. As increased insulin resistance, rather than beta cell function, is related to an insufficient response to a low carbohydrate diet, we speculate that insulin sensitizers rather than insulin therapy may be the most targeted therapeutic modality in diet-insensitive GDM.
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spelling pubmed-92312082022-06-25 Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus Ellerbrock, Jonas Spaanderman, Benthe van Drongelen, Joris Mulder, Eva Lopes van Balen, Veronica Schiffer, Veronique Jorissen, Laura Alers, Robert-Jan Leenen, Jeanine Ghossein-Doha, Chahinda Spaanderman, Marc Nutrients Article Background: Gestational diabetes mellitus (GDM) is a pregnancy complication characterized by second trimester hyperglycemia. Untreated, GDM is related to an increased risk for adverse pregnancy outcomes. Both beta cell dysfunction and insulin resistance underlie impaired glucose tolerance. Understanding the dominant mechanism predisposing to GDM may be important to provide effective treatment in order to improve perinatal outcomes. We hypothesize that insulin resistance rather that beta cell dysfunction predisposes to GDM. Methods: A 75g oral glucose tolerance test (OGTT) was performed on 2112 second-trimester pregnant women to determine the relationship between insulin resistance (HOMA-IR), beta cell function (HOMA-β), and the prevalence of abnormal glucose handling. Results: High insulin resistance raised the risk of GDM (relative risk (RR) 6.1, 95% confidence interval (CI) (4.4–8.5)), as did beta cell dysfunction (RR 3.8, 95% CI (2.7–5.4)). High insulin resistance, but not beta cell function, enhances the necessity for additional glucose lowering medication on top of a low carbohydrate diet in women diagnosed with GDM. Conclusions: Both high insulin resistance and beta cell dysfunction increase the risk of GDM. As increased insulin resistance, rather than beta cell function, is related to an insufficient response to a low carbohydrate diet, we speculate that insulin sensitizers rather than insulin therapy may be the most targeted therapeutic modality in diet-insensitive GDM. MDPI 2022-06-13 /pmc/articles/PMC9231208/ /pubmed/35745174 http://dx.doi.org/10.3390/nu14122444 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Ellerbrock, Jonas
Spaanderman, Benthe
van Drongelen, Joris
Mulder, Eva
Lopes van Balen, Veronica
Schiffer, Veronique
Jorissen, Laura
Alers, Robert-Jan
Leenen, Jeanine
Ghossein-Doha, Chahinda
Spaanderman, Marc
Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title_full Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title_fullStr Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title_full_unstemmed Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title_short Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus
title_sort role of beta cell function and insulin resistance in the development of gestational diabetes mellitus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231208/
https://www.ncbi.nlm.nih.gov/pubmed/35745174
http://dx.doi.org/10.3390/nu14122444
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