Gut Microbiota: Novel Therapeutic Target of Ginsenosides for the Treatment of Obesity and Its Complications

Tongxi Zhuang,Lili Ding,Mingmei Zhou,Zhengtao Wang,Wei Li,Li Yang

doi:10.3389/fphar.2021.731288

Abstract

Obesity, generally characterized by excessive lipid accumulation, is a metabolic threat worldwide due to its rapid growth in global prevalence. Ginsenosides are crucial components derived from natural plants that can confer metabolic benefits for obese patients. Considering the low bioavailability and degradable properties of ginsenosides in vivo, it should be admitted that the mechanism of ginsenosides on anti-obesity contribution is still obscure. Recently, studies have indicated that ginsenoside intervention has beneficial metabolic effects on obesity and its complications because it allows for the correction of gut microbiota dysbiosis and regulates the secretion of related endogenous metabolites. In this review, we summarize the role of gut microbiota in the pathogenetic process of obesity, and explore the mechanism of ginsenosides for ameliorating obesity, which can modulate the composition of gut microbiota by improving the metabolism of intestinal endogenous substances and alleviating the level of inflammation. Ginsenosides are expected to become a promising anti-obesity medical intervention in the foreseeable clinical settings.

Highlights

Obesity, a complicated chronic metabolic disorder (An et al, 2020), causes visual changes in humans, alongside the excessive accumulation of adipose tissue (Hammarstedt et al, 2018; Ruiz-Ojeda et al, 2019)
Gut microbiota disorders can activate intestinal epidermal growth factors, which directly act on protease activated receptors, cripple intestinal tight junctions (TJ) structure, significantly down-regulate the expression of TJ protein zonula occludens 1 (ZO-1), eventually destroying the structure of intestinal barrier and increasing the amount of lipopolysaccharide entering the blood from the intestinal tract (Guo et al, 2013; Pontarollo et al, 2020)
This process increased the secretion of taurolithocholic acid (TLCA), fibroblast growth factor 15 (FGF15) and glucagon like peptide 1 (GLP-1), which stimulated TGR5 expression in the intestine, promoted the secretion of GLP-1, improved insulin and glucose tolerance, and promoted the browning of white adipose tissue in mice (Pathak et al, 2018)

Summary

INTRODUCTION

A complicated chronic metabolic disorder (An et al, 2020), causes visual changes in humans, alongside the excessive accumulation of adipose tissue (Hammarstedt et al, 2018; Ruiz-Ojeda et al, 2019). Gut microbiota disorders can activate intestinal epidermal growth factors, which directly act on protease activated receptors, cripple intestinal TJ structure, significantly down-regulate the expression of TJ protein zonula occludens 1 (ZO-1), eventually destroying the structure of intestinal barrier and increasing the amount of lipopolysaccharide entering the blood from the intestinal tract (Guo et al, 2013; Pontarollo et al, 2020). Another study found that acetylation factors and Bacteroides were increased in the intestine of mice treated with fexaramine (an FXR agonist) This process increased the secretion of taurolithocholic acid (TLCA), fibroblast growth factor 15 (FGF15) and glucagon like peptide 1 (GLP-1), which stimulated TGR5 expression in the intestine, promoted the secretion of GLP-1, improved insulin and glucose tolerance, and promoted the browning of white adipose tissue in mice (Pathak et al, 2018).

DISCUSSION

CONCLUDING REMARKS