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.

我们展示了 C3G（一种主要的膳食花青素）调节能量代谢和胰岛素敏感性的机制。在高脂肪饮食喂养的小鼠中，口服 C3G 可降低肝脏和血浆甘油三酯水平、肥胖并改善葡萄糖耐量。肝脏代谢组学分析显示，C3G 将代谢物谱转向脂肪酸氧化和生酮。C3G 增加了 HepG2 细胞和 C2C12 肌管中的葡萄糖摄取，并诱导了肝脏脂肪酸氧化的速率。C3G 直接与 PPAR 相互作用并激活它，对 PPARα 的亲和力最高。C3G 降低血浆和肝脏甘油三酯、葡萄糖耐量和肥胖以及诱导氧消耗和能量消耗的能力在 PPARα 缺陷小鼠中被废除，表明 PPARα 是 C3G 的主要目标。这些发现表明，膳食花青素 C3G 会激活 PPAR，它是能量代谢的主要调节剂。C3G 是 PPAR 的激动配体，可刺激燃料对脂肪的偏好。