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Dietary supplementation of inulin alleviates metabolism disorders in gestational diabetes mellitus mice via RENT/AKT/IRS/GLUT4 pathway

内分泌学 内科学 过剩4 妊娠期糖尿病 医学 糖尿病 碳水化合物代谢 蛋白激酶B PI3K/AKT/mTOR通路 胰岛素抵抗 代谢紊乱 生物信息学 怀孕 信号转导 生物 妊娠期 生物化学 遗传学
作者
Miao Miao,Yongmei Dai,Can Rui,Yuru Fan,Xinyan Wang,Chong Fan,Juan Mu,Wenwen Hou,Zhiyong Dong,Ping Li,Guiju Sun,Xin Zeng
出处
期刊:Diabetology & Metabolic Syndrome [BioMed Central]
卷期号:13 (1): 150-150 被引量:26
标识
DOI:10.1186/s13098-021-00768-8
摘要

Abstract Background Gestational diabetes mellitus (GDM) has significant short and long-term health consequences for both the mother and child. There is limited but suggestive evidence that inulin could improve glucose tolerance during pregnancy. This study assessed the effect of inulin on glucose homeostasis and elucidated the molecular mechanisms underlying the inulin-induced antidiabetic effects during pregnancy. Method Female C57BL/6 mice were randomized to receive either no treatment, high-dose inulin and low-dose inulin for 7 weeks with measurement of biochemical profiles. A real-time 2 (RT 2 ) profiler polymerase chain reaction (PCR) array involved in glycolipid metabolism was measured. Results Inulin treatment facilitated glucose homeostasis in a dose-dependent manner by decreasing fasting blood glucose, advanced glycation end products and total cholesterol, and improving glucose tolerance. Suppressing resistin (RETN) expression was observed in the inulin treatment group and the expression was significantly correlated with fasting blood glucose levels. The ratios of p-IRS to IRS and p-Akt to Akt in liver tissue and the ratio of p-Akt to Akt in adipose tissue as well as the expression level of GLUT4 increased significantly after inulin treatment. Conclusions Our findings indicated improvement of glucose and lipid metabolism by inulin was to activate glucose transport through the translocation of GLUT4 which was mediated by insulin signaling pathway repairment due to decreased expression of RETN and enhanced phosphorylation of IRS and Akt in GDM mice.
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