ArticleReproductive sciences (Thousand Oaks, Calif.)2024
Contribution of Insulin Resistance and β Cell Dysfunction to Gestational Diabetes Stratified for Pre-pregnant Body Mass Index.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Association of CDKAL1 rs7754840 with gestational diabetes mellitus: a systematic review and meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Article
- Upregulation of hepatic flavin-containing monooxygenase 3 by increased corticosterone via glucocorticoid receptor contributes to gestational diabetes mellitus.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- PREGNANCY DISORDERS AND MATERNAL CONSEQUENCES: Maternal pre-pregnancy risks and postpartum consequences of gestational diabetes.Reproduction (Cambridge, England) · 2025Review
- Unveiling Gestational Diabetes: An Overview of Pathophysiology and Management.International journal of molecular sciences · 2025Review
- Adiponectin C1Q and Collagen Domain Containing rs266729, Cyclin-Dependent Kinase Inhibitor 2A and 2B rs10811661, and Signal Sequence Receptor Subunit 1 rs9505118 Polymorphisms and Their Association with Gestational Diabetes Mellitus: A Case-Control Study in a Romanian Population.International journal of molecular sciences · 2025Article
- Matsuda index adjusted for sustained hyperglycemia via propensity scores outperforms homeostatic model assessment for insulin resistance in identifying insulin-requiring gestational diabetes mellitus.SAGE open medicine · 2025Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
The objective of the study was to evaluate the contribution of insulin resistance and β cell dysfunction to gestational diabetes mellitus (GDM) in Chinese women stratified by pre-pregnant body mass index (BMI). A total of 847 pregnant women were enrolled. They were divided into low BMI and high BMI groups according to the median of pre-pregnancy BMI. The homeostasis model assessment of insulin resistance (HOMA-IR) and β cell function (HOMA-β), Matsuda index, and 60-min insulinogenic index (IGI60) were used to evaluate insulin resistance and β cell function. In all the participants, 150 (17.71%) were diagnosed with GDM. ROC analyses showed that in the low BMI group, the association of β cell dysfunction (IGI60 or HOMA-β) with GDM was stronger than that of insulin resistance (Matsuda index or HOMA-IR), while in the high BMI group, the association of β cell dysfunction with GDM was weaker than that of insulin resistance (all P < 0.05). Among all GDM patients, 47.33% demonstrated predominant insulin resistance (Matsuda index < 25th percentile), and 46% had predominant β cell defect (IGI60 < 25th percentile). In the low BMI group, 15.09% of GDM patients demonstrated predominant insulin resistance, and 62.26% of GDM patients had predominant β cell defect, whereas in the high BMI group, 64.95% of GDM patients demonstrated mainly insulin resistance and 36.08% of GDM patients had mainly β cell defect. In women with low BMI, β cell dysfunction is the major etiologic factor, whereas, in women with high BMI, insulin resistance is the predominant etiologic factor in the development of GDM.
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