Green tea extract increases adiponectin and PPAR α levels to improve hepatic steatosis

We postulated that Green tea (GT) improvements in non-alcoholic fatty liver disease (NAFLD) are dependent on adiponectin action in the liver. Male wild-type and adiponectin knockout (adipoKO) mice were induced to obesity for 8 weeks with a high-fat diet and then treated with GT for the last 12 weeks of the experimental protocol. Glucose and insulin tolerance tests, indirect calorimetry, histologic analysis of liver sections, and quantification of mRNA of hepatic genes related to glucose or fatty acid metabolism were performed. In vitro, we assessed the mechanism by which GT catechins act to improve hepatic steatosis by measuring lipid accumulation, and transcript levels of lipogenic genes in HepG2 cells treated with GT in the presence of a PPAR antagonist. Additionally, we performed a PPAR transactivation assay in 293T cells to test if catechins could activate PPARs. Different from wild-type mice, adipoKO animals treated with GT and fed a HFD gain body weight and fat mass, that were associated with a decrease in energy expenditure, were insulin resistant, and had no improvements in hepatic steatosis. Increased lipid levels were associated with no modulation of PPAR alpha levels in the liver of adipoKO mice treated with GT. In vitro, we demonstrated GT catechins act to reduce hepatic steatosis in a PPAR alpha-dependent manner, and especially epigallocatechin and epicatechin can indirectly activate PPAR alpha, although it seems they are not direct ligands. By providing the mechanisms by which GT catechins act in the liver to improve steatosis, our data contribute to the discovery of novel therapeutic agents in the management of NAFLD. (C) 2022 Elsevier Inc. All rights reserved.

Automated summary

This study demonstrates that green tea can improve non-alcoholic fatty liver disease (NAFLD), and this improvement is dependent on the action of adiponectin in the liver. The researchers found that catechins in green tea can reduce hepatic steatosis in a PPAR alpha-dependent manner.