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Sodium Butyrate Improves Liver Glycogen Metabolism in Type 2 Diabetes Mellitus

Wen-Qian Zhang, Ting-Ting Zhao, Ding-Kun Gui, Chen-Lin Gao, Jun-Ling Gu, Wen-Jun Gan, Wei Huang, Yong Xu, Hua Zhou, Wei-Ni Chen, Zhi-Long Liu, You-Hua Xu

J Agric Food Chem. 2019 Jul 10;67(27):7694-7705.

PMID: 31250637

Abstract:

Liver plays a central role in modulating blood glucose level. Our most recent findings suggested that supplementation with microbiota metabolite sodium butyrate (NaB) could ameliorate progression of type 2 diabetes mellitus (T2DM) and decrease blood HbA1c in db/db mice. To further investigate the role of butyrate in homeostasis of blood glucose and glycogen metabolism, we carried out the present study. In db/db mice, we found significant hypertrophy and steatosis in hepatic lobules accompanied by reduced glycogen storage, and expression of GPR43 was significantly decreased by 59.38 ± 3.33%; NaB administration significantly increased NaB receptor G-protein coupled receptor 43 (GPR43) level and increased glycogen storage in both mice and HepG2 cells. Glucose transporter 2 (GLUT2) and sodium-glucose cotransporter 1 (SGLT1) on cell membrane were upregulated by NaB. The activation of intracellular signaling Protein kinase B (PKB), also known as AKT, was inhibited while glycogen synthase kinase 3 (GSK3) was activated by NaB in both in vivo and in vitro studies. The present study demonstrated that microbiota metabolite NaB possessed beneficial effects on preserving blood glucose homeostasis by promoting glycogen metabolism in liver cells, and the GPR43-AKT-GSK3 signaling pathway should contribute to this effect.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP156547-A Sodium butyrate Sodium butyrate 156-54-7 Price
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