Dietary Epigallocatechin-3-Gallate Alters the Gut Microbiota of Obese Diabetic db/db Mice: Lactobacillus Is a Putative Target

Abstract

Obesity results in the progression of metabolic disorders, and especially type 2 diabetes mellitus (T2DM), and the gut microbiota have been implicated in the development of T2DM. This study investigated the effect of epigallocatechin-3-gallate (EGCG) on structural changes to the gut microbiota of obese diabetic db/db mice. db/db mice were subjected to a control and EGCG (10, 50, and 100 mg/kg) diet for 8 weeks. Glucose homeostasis and the structure and composition of the gut microbiota were measured. EGCG inhibited the increases in body weight and fasting blood glucose levels. Similarly, it resulted in remarkable improvements in glucose tolerance. Based on lipid profiles, EGCG decreased serum cholesterol and low-density lipoprotein (LDL) levels, and increased the high-density lipoprotein/LDL ratio. In addition, upon fecal microbiota analysis, this compound significantly increased the Firmicutes:Bacteroidetes ratio at the phylum level and increased Lactobacillus abundance at the genus level. Especially, its administration increased abundances of the Lactobacillus gasseri, Lactobacillus intestinalis, and Lactobacillus reuteri. We also found that EGCG increased Christensenellaceae abundance and decreased Enterobacteriaceae and Proteobacteria abundance at the family level. EGCG improves glucose homeostasis in diabetic mice. Its beneficial effects on glucose homeostasis are likely associated with alterations to the gut microbiota. Furthermore, the enrichment of probiotics (Lactobacillus) might be a potential mechanism underlying the effects of EGCG on glucose homeostasis.