Bai H. New exploration on pathogenesis and early diagnosis of gestational diabetes. World J Clin Cases 2025; 13(1): 93826 [DOI: 10.12998/wjcc.v13.i1.93826]
Corresponding Author of This Article
Hua Bai, MD, PhD, Chief, Full Professor, Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, No. 172 JianJiangbei Road, Duyun 558099, Guizhou Province, China. baih2020@gmc.edu.cn
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Cases. Jan 6, 2025; 13(1): 93826 Published online Jan 6, 2025. doi: 10.12998/wjcc.v13.i1.93826
New exploration on pathogenesis and early diagnosis of gestational diabetes
Hua Bai
Hua Bai, Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, Duyun 558099, Guizhou Province, China
Author contributions: Bai H study conception and design, data collection, paper writing and paper revision.
Supported by National Natural Science Foundation of China, No. 32060182; and Qiannan Prefecture Science and Technology Plan Project in China: Qiannan Kehe She Zi [2022] No. 1.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hua Bai, MD, PhD, Chief, Full Professor, Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, No. 172 JianJiangbei Road, Duyun 558099, Guizhou Province, China. baih2020@gmc.edu.cn
Received: March 6, 2024 Revised: July 22, 2024 Accepted: July 25, 2024 Published online: January 6, 2025 Processing time: 245 Days and 22.9 Hours
Abstract
Gestational diabetes mellitus (GDM) refers to varying degrees of abnormal glucose metabolism that occur during pregnancy and excludes patients previously diagnosed with diabetes. GDM is a unique among the four subtypes of diabetes classified by the international World Health Organization standards. Although GDM patients constitute a small proportion of the total number of diabetes cases, the incidence of GDM has risen significantly over the past decade, posing substantial risk to pregnant women and infants. Therefore, it warrants considerable attention. The pathogenesis of GDM is generally considered to resemble that of type II diabetes, though it may have distinct characteristics. Analyzing blood biochemical proteins in the context of GDM can help elucidate its pathogenesis, thereby facilitating more effective prevention and management strategies. This article reviews this critical clinical issue to enhance the medical community's sufficient understanding of GDM.
Core Tip: Pancreas β cellular damage and tissue insulin resistance are key to the pathogenesis of gestational diabetes mellitus (GDM). Once beta cell dysfunction begins, hyperglycemia, insulin resistance, and further beta cell dysfunction are likely to enter a vicious cycle. Introducing advanced biotechnology such as proteomics for basic research on GDM is a good attempt. RBP4 and ANGPTL8 proteins may play a role in the pathogenesis of GDM, but there is insufficient evidence to diagnose GDM by detecting the two proteins.
