Diabetes & Metabolism Journal

Original Articles

Metabolic Risk/Epidemiology
Pregravid Weight Gain Is Associated with an Increased Risk of Gestational Diabetes: Sunmie Kim, Kyungdo Han, Su-Yeon Choi, Min Joo Kim, Sun Young Yang, Seung Ho Choi, Jeong Yoon Yim, Jin Ju Kim, Min-Jeong Kim; Received August 19, 2024 Accepted November 15, 2024 Published online March 26, 2025; DOI: https://doi.org/10.4093/dmj.2024.0491 [Epub ahead of print]

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Background
Studies have reported a significant association between pregravid weight gain and the subsequent development of gestational diabetes mellitus (GDM) in various populations. The current study aims to investigate this relationship using data from the Korean National Health Insurance Service database.
Methods
We conducted a retrospective nationwide population-based cohort study, involving 159,798 women who gave birth between 2015 and 2017 and had undergone two national health screening examinations: 1 year (index checkup) and 3 years before (baseline checkup) their respective estimated conception date. Participants were categorized into five groups based on the extent of weight change between the two examinations: more than 10%, 5% to 10%, –5% to 5% (reference group), –10% to –5%, and more than –10%. The study assessed the association between pregravid weight change and GDM risk.
Results
Among the 146,363 women analyzed, 11,012 (7.52%) were diagnosed with GDM. Multiple regression analysis revealed that women who gained 5% to 10% of their weight had a 12% increased risk of GDM (adjusted odds ratio [aOR], 1.12; 95% confidence interval [CI], 1.06 to 1.17), while those who gained ≥10% had a 34% higher risk (aOR, 1.34; 95% CI, 1.26 to 1.43). Notably, pregravid weight gain was particularly associated with GDM risk in non-obese or non-metabolic syndrome groups at index checkup.
Conclusion
Pregravid weight gain showed a dose-dependent association with a higher risk of GDM. This association was more pronounced in non-obese individuals emphasizing the importance of minimizing pregravid weight gain for GDM prevention, even in non-obese women.

Citations

Citations to this article as recorded by

Advancing Early Prediction of Gestational Diabetes Mellitus with Circular RNA Biomarkers
Joon Ho Moon, Sung Hee Choi
Diabetes & Metabolism Journal.2025; 49(3): 403. CrossRef

Basic Research
Glucagon-Like Peptide Receptor Agonist Inhibits Angiotensin II-Induced Proliferation and Migration in Vascular Smooth Muscle Cells and Ameliorates Phosphate-Induced Vascular Smooth Muscle Cells Calcification: Jinmi Lee, Seok-Woo Hong, Min-Jeong Kim, Sun Joon Moon, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Won-Young Lee; Diabetes Metab J. 2024;48(1):83-96. Published online January 3, 2024; DOI: https://doi.org/10.4093/dmj.2022.0363

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Background
Glucagon-like peptide-1 receptor agonist (GLP-1RA), which is a therapeutic agent for the treatment of type 2 diabetes mellitus, has a beneficial effect on the cardiovascular system.
Methods
To examine the protective effects of GLP-1RAs on proliferation and migration of vascular smooth muscle cells (VSMCs), A-10 cells exposed to angiotensin II (Ang II) were treated with either exendin-4, liraglutide, or dulaglutide. To examine the effects of GLP-1RAs on vascular calcification, cells exposed to high concentration of inorganic phosphate (Pi) were treated with exendin-4, liraglutide, or dulaglutide.
Results
Ang II increased proliferation and migration of VSMCs, gene expression levels of Ang II receptors AT1 and AT2, proliferation marker of proliferation Ki-67 (Mki-67), proliferating cell nuclear antigen (Pcna), and cyclin D1 (Ccnd1), and the protein expression levels of phospho-extracellular signal-regulated kinase (p-Erk), phospho-c-JUN N-terminal kinase (p-JNK), and phospho-phosphatidylinositol 3-kinase (p-Pi3k). Exendin-4, liraglutide, and dulaglutide significantly decreased the proliferation and migration of VSMCs, the gene expression levels of Pcna, and the protein expression levels of p-Erk and p-JNK in the Ang II-treated VSMCs. Erk inhibitor PD98059 and JNK inhibitor SP600125 decreased the protein expression levels of Pcna and Ccnd1 and proliferation of VSMCs. Inhibition of GLP-1R by siRNA reversed the reduction of the protein expression levels of p-Erk and p-JNK by exendin-4, liraglutide, and dulaglutide in the Ang II-treated VSMCs. Moreover, GLP-1 (9-36) amide also decreased the proliferation and migration of the Ang II-treated VSMCs. In addition, these GLP-1RAs decreased calcium deposition by inhibiting activating transcription factor 4 (Atf4) in Pi-treated VSMCs.
Conclusion
These data show that GLP-1RAs ameliorate aberrant proliferation and migration in VSMCs through both GLP-1Rdependent and independent pathways and inhibit Pi-induced vascular calcification.

Citations

Citations to this article as recorded by

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