Modulating the expression of genes associated with hepatic lipid metabolism, lipoperoxidation and inflammation by cocoa, cocoa extract and cocoa flavanols related to hepatic steatosis induced by a hypercaloric diet

- Cocoa flavanols decrease intra-abdominal fat mass accumulation and liver weight.
- CD36, PPARγ downregulation by flavanols contributes to decrease fatty acid uptake
- ACC downregulation by flavanols contributes to decrease hepatic de novo lipogenesis
- PPARα, PGC1α, SIRT1 upregulation by flavanols diminish hepatic triglyceride content
- Cocoa flavanols reduce liver inflammation by downregulation of TNF-α, Il-6 and TLR4

Cocoa and its bioactive compounds are widely known for its beneficial effects as attenuate insulin resistance, hepatic lipid deposition, inflammation and oxidative stress induced by hypercaloric diets. The present in vivo study investigated the effects of cocoa powder, cocoa extract and its main flavanols (epicatechin, catechin and procyanidin B2) on the expression of genes involved in the regulation of hepatic lipid metabolism, lipoperoxidation and inflammation associated to hepatic steatosis induced by a hypercaloric diet. This study demonstrates that oral treatment with cocoa powder, cocoa extract and cocoa flavanols significantly attenuate hepatic steatosis induced by hypercaloric feeding, in part, through downregulation of genes involved in hepatic fatty acid uptake (PPARγ, CD36) and lipogenesis (ACC) and upregulation of key regulators of mitochondrial function (PPARα, SIRT1) and FA oxidation (PGC-1α) as well as in attenuating hepatic oxidative stress and inflammation by upregulating hepatic antioxidant enzymes and decreasing gene expression of proinflammatory cytokines (TNF-α, IL-6).