n/a
Abstract Title:

LC89 exerts antidiabetic effects through regulating hepatic glucagon response and gut microbiota in type 2 diabetic mice.

Abstract Source:

Food Funct. 2021 Sep 20 ;12(18):8288-8299. Epub 2021 Sep 20. PMID: 34308462

Abstract Author(s):

Yongli Zhang, Tao Wu, Wen Li, Yunjiao Zhao, Hairong Long, Rui Liu, Wenjie Sui, Min Zhang

Article Affiliation:

Yongli Zhang

Abstract:

Previous study suggests thatexhibits antihyperglycemic activity, however, the molecular mechanism of this has yet to be elucidated. Here, the anti-diabetic effects and underlying mechanisms ofLC89 are investigated in type 2 diabetes mellitus (T2DM) mice, which was induced by a high-fat diet (HFD) with streptozotocin (100 mg per kg BW). The results show that LC89 at a dose of 10CFU daydecreases fasting blood glucose (FBG) and insulin levels by 35.12% and 28.37%, respectively, compared to the diabetes control (DC) group. Moreover, LC89 treatment improved the insulin resistance index (HOMA-IR), serum lipid profiles and inflammation cytokines. The real-time polymerase chain reaction indicated that LC89 markedly downregulates the mRNA expression of hepatic glucagon (GCG), glucagon receptor (GCGR), phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). Meanwhile, LC89 significantly decreases the abundance of, but increases the,,andcontent. Therefore, LC89 plays a positive role in alleviating T2DM by regulating gut microbiota and glucagon signal pathway-related genes, and it may be a beneficial dietary supplement to regulate glucose metabolism in T2DM.

Study Type : Animal Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.