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Contribution of Insulin Resistance and β Cell Dysfunction to Gestational Diabetes Stratified for Pre-pregnant Body

Qingrong Pan1, Yanna Yang2,3, Huawei Cao4

  • 1Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, No. 8, Gongti South Road, Chaoyang District, Beijing, 100020, China.

Reproductive Sciences (Thousand Oaks, Calif.)
|November 13, 2023
PubMed

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.

Keywords:
Body mass indexGestational diabetesInsulin resistanceβ cell dysfunction

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