1. A dietary anthocyanin cyanidin-3-O-glucoside binds to PPARs to regulate glucose metabolism and insulin sensitivity in mice.
- Author
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Jia Y, Wu C, Kim YS, Yang SO, Kim Y, Kim JS, Jeong MY, Lee JH, Kim B, Lee S, Oh HS, Kim J, So MY, Yoon YE, Thach TT, Park TH, and Lee SJ
- Subjects
- Animals, Anthocyanins pharmacology, Dietary Supplements, Energy Metabolism genetics, Glucose genetics, Hep G2 Cells, Humans, Insulin genetics, Insulin metabolism, Insulin Resistance genetics, Lipid Metabolism genetics, Liver metabolism, Mice, Anthocyanins genetics, Mediator Complex Subunit 1 genetics, Peroxisome Proliferator-Activated Receptors genetics
- Abstract
We demonstrate the mechanism by which C3G, a major dietary anthocyanin, regulates energy metabolism and insulin sensitivity. Oral administration of C3G reduced hepatic and plasma triglyceride levels, adiposity, and improved glucose tolerance in mice fed high-fat diet. Hepatic metabolomic analysis revealed that C3G shifted metabolite profiles towards fatty acid oxidation and ketogenesis. C3G increased glucose uptake in HepG2 cells and C2C12 myotubes and induced the rate of hepatic fatty acid oxidation. C3G directly interacted with and activated PPARs, with the highest affinity for PPARα. The ability of C3G to reduce plasma and hepatic triglycerides, glucose tolerance, and adiposity and to induce oxygen consumption and energy expenditure was abrogated in PPARα-deficient mice, suggesting that PPARα is the major target for C3G. These findings demonstrate that the dietary anthocyanin C3G activates PPARs, a master regulators of energy metabolism. C3G is an agonistic ligand of PPARs and stimulates fuel preference to fat.
- Published
- 2020
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