Visfatin level and gestational diabetes mellitus: a systematic review and meta-analysis.

It is reported that elevated visfatin level is associated with gestational diabetes mellitus (GDM). However, the relationship between visfatin level and GDM remains controversial. The aim of our study was to systematically review available literature linking visfatin to GDM for a comprehensive understanding of the relationship between circulating visfatin level and GDM in human. PubMed, The Cochrane Library and Web of Science were searched for studies published up to July 2020. Standard mean difference with 95% confidence interval was calculated to evaluate the relationship between visfatin level and GDM using the Review Manager 5.3 and Stata 12.0. The evidence indicated that no significant difference was observed in the level of circulating visfatin between the women with GDM and normal glucose tolerance, suggesting circulating visfatin level is not independently related to GDM. Nevertheless, visfatin is involved in the development of GDM in obese women.

Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice.

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.