• Curcumin alleviated hepatic steatosis and insulin resistance in obese mice.
  • Curcumin increased abundance of Bacteroides, Parabacteroides, Alistipes and Alloprevotella.
  • Curcumin increased the caecal and colonic short chain fatty acids (SCFA) contents.
  • Curcumin reduced endotoxin-producing Desulfovibrio bacteria and circulating serum LPS.
  • The dominant bacterial taxa altered by Curcumin were related with improvement of obesity.

Curcumin is a natural polyphenol with beneficial effect against obesity and related metabolic disorders.

We see that gut microbiota may be a prospective therapeutic target for Cur-induced metabolic benefits. The metabolic adaptations resulting from Curcumin supplementation were mediated by the gut microbiota in high-fat diet (HFD)-fed obese mice. C57BL/6 mice were fed a control diet or a HFD diet with or without 0.2% Curcumin for 10 weeks.

Lipid profiles, insulin sensitivity, hepatic metabolism, gut microbiota composition and short-chain fatty acid (SCFA) production were determined. Dietary Curcumin reduced fat mass, hepatic steatosis and circulating lipopolysaccharide levels and improved the insulin sensitivity in HFD-fed mice.

More importantly, Curcumin supplementation modulated the gut microbiota composition and ameliorated intestinal dysbiosis by decreasing the ratio of Firmicutes/Bacteroidetes and endotoxin-producing Desulfovibrio bacteria and increasing the abundance of Akkermansia population and SCFA-producing bacteria, such as Bacteroides, Parabacteroides, Alistipes and Alloprevotella, along with increases in caecal and colonic SCFA concentrations. These dominant bacterial genera altered by Cur showed strong correlations with the obesity-related metabolic parameters in HFD-fed mice. In conclusion, our data suggest that Cur alleviated metabolic features of hepatic steatosis and insulin resistance in HFD-fed obese mice, which might be associated with the modulation of gut microbiota composition and metabolites.

Curcumin also induces secretion of glucagon-like peptide-1 (GLP-1). GLP-1 and glucose-dependent insulinotropic peptide (GIP) are incretin hormones that are released in response to oral nutrient ingestion as potent inducers of insulin secretion.

Incretins also protect pancreatic beta cells from damage, and GLP-1 may induce beta cell regeneration. Their effects on glucose homeostasis make the incretins potential therapeutic targets for the management of diabetes mellitus.

Curcumin may function as a potential GLP-1 secretagogue since it induced GLP-1 secretion in an in vitro cell line and in rats resulting in improved glucose control.