Overview of the role of “Gut microbiota-adipose tissue axis” in the anti-obesity benefits of resveratrol. SCFAs, short-chain fatty acids; AMPK, AMP-activated protein kinase; SIRT1, sirtuin1; UCP1, uncouple protein 1; PGC1α, PPARγ coactivator 1 alpha; PRDM16, PRD1-BF-1-RIZ1 homologous domain protein containing protein 16; WAT, white adipose tissue.
Resveratrol, a polyphenolic compound with prebiotic properties, can be metabolized by gut microbiota to produce metabolites, such as dihydroresveratrol and lunularin.
Interestingly, numerous studies have shown that resveratrol has the potential to modulate the composition of gut microbiota, and this is related to its anti-obesity effects and its improvement of metabolic effects.
Effects of resveratrol on gut microbiota were first detected in an obese mouse model induced by a high-fat diet and the results showed that resveratrol intake significantly improved the gut microbial dysbiosis in high-fat diet group and decreased body and fat weight.
The Bacteroidetes/Firmicutes ratios, which is decreased during the development of obesity, and the abundances of Lactobacillus and Bifidobacterium, were significantly increased, whereas, the abundance of Enterococcus faecalis was decreased after resveratrol intervention.
Subsequently, another study also showed that the Bacteroidetes/Firmicutes ratio was significantly increased in resveratrol-treated mice with a high-fat diet. In addition, increases in the abundances of Parabacteroides, Bilophila, and Akkermansia and a decrease in the relative abundance of Lachnospiraceae were observed in high-fat diet fed mice with resveratrol.
A significant increase in the relative abundances of Bacteroides, Lactobacillus, Bifidobacterium, and Akkermansia and a decrease in the Prevotella, Ruminococcaceae, Anaerotruncus, Alistipes, Helicobacter, and Peptococcaceae were also identified in mice with trimethylamine-N-oxide (TMAO)-induced atherosclerosis treated with resveratrol.
Subsequently, several experimental animal studies confirmed that resveratrol might regulate body weight and metabolism via modifying gut microbiota. In one study, the results showed that resveratrol intake (0.4%) influenced the gut microbial composition only in obese mice and not in standard diet-fed mice, which was consistent with the positive effects of resveratrol on body weight and metabolism observed in obese animals fed an obesogenic diet.
Resveratrol, has been widely accepted as an anti-obesity agent and a metabolic effector.
A multitude of evidence has demonstrated that stimulating WAT browning through the AMPK-SIRT1-PGC1α pathway or the cAMP signaling pathway is one of the critical mechanisms that is utilized by resveratrol to combat obesity.
In addition, resveratrol has been confirmed to have prebiotic properties and was not only metabolized by gut microbiota but also influenced the composition of the gut microbial community.
The significant role of gut microbiota in inducing WAT browning has also been well established through correlation analysis, fecal transplantation experiments and microbiota-depleted animal models.
Microbiota-derived metabolites, especially the SCFAs, might be the key to mediating the crosstalk between gut microbiota and WAT browning. Therefore, we conclude that resveratrol induces the browning of WAT through modulating the composition of gut microbiota and their metabolites, which play a vital role in anti-obesity effects. In other words, the “gut microbiota-adipose tissue” axis might be the key to elucidating the anti-obesity benefits of resveratrol.
The interaction of Resveratrol and gut bacteria have been shown to increase GLP-1 Levels.
The maximum amount of Resveratrol that will dissolve in a glass of water has been included that is 6mg. Currently no Water soluble Resveratrol is available unlike Curcumin.