Diabetes Metab Syndr Obes. 2019 Oct 14;12:2095-2105. doi: 10.2147/DMSO.S221396. eCollection 2019.
Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice.
Diabetes, metabolic syndrome and obesity : targets and therapy
Yong-Kuan Jiang, Kai-Yue Xin, Hong-Wei Ge, Fei-Juan Kong, Gang Zhao
Affiliations
Affiliations
- Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang, People's Republic of China.
- Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
- Department of Cardiology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People's Republic of China.
- Department of Urology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
- Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
- Department of Endocrinology and Metabolism, Xuhui District Central Hospital of Shanghai, Shanghai, People's Republic of China.
- Department of Cardiology, Kashgar Prefecture Second People's Hospital, Kashi, Xinjiang, People's Republic of China.
PMID: 31686881
PMCID: PMC6800457 DOI: 10.2147/DMSO.S221396
Abstract
INTRODUCTION: Gestational diabetes mellitus (GDM) is a metabolic disorder during mid- to late-pregnancy characterized by hyperglycemia, insulin resistance and fetal mal-development. Glucose transporter type 2 (GLUT2) and sodium-coupled glucose cotransporters 2 (SGLT2) in the proximal tubules play a critical role in the reabsorption of glucose and have been linked to the occurrence of type 2 diabetes mellitus (T2DM). Our study was designed to investigate the role of GLUT2 and SGLT2 in the pathogenesis of GDM, which is considered a forerunner of T2DM, and investigate the related molecular mechanism.
METHODS: High-fat diet (HFD) was utilized to build a GDM mouse model that closely induces metabolic abnormalities similar to human GDM. Body weight, blood glucose and serum insulin were recorded in the experimental process. Glucose tolerance was determined by the use of an intraperitoneal glucose tolerance test (IPGTT). In addition, levels of GLUT2 and SGLT2 were evaluated to further explore the underlying mechanism of GDM.
RESULTS: HFD feeding induced abnormal glucose metabolism as manifested by increased levels of blood glucose and insulin and prominent glucose intolerance. Additionally, fetal mice from mother feed on HFD showed higher mean body weight. Furthermore, HFD feeding led to an increase in the number of positive cells of GLUT2 and SGLT2 in the renal proximal tubule and the expressions of renal GLUT2 and SGLT2 mRNA and proteins in mice. However, no obvious change was observed in renal morphology.
CONCLUSION: Our study demonstrates a potential involvement of renal GLUT2 and SGLT2 in GDM pathology in an HFD-induced GDM mouse model, which further supports the role of renal GLUT2 and SGLT2 not only in T1DM and T2DM but also in GDM.
© 2019 Jiang et al.
Keywords: GLUT2; SGLT2; gestational diabetes mellitus; insulin resistance; renal threshold for glucose
Conflict of interest statement
The authors declare no conflicts of interest, financial or otherwise in this work.
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