Salubrious Effects of Green Tea Catechins on Fatty Liver Disease: A Systematic Review

Abstract

Epigallocatechin-3-gallate (EGCG) is a polyphenol green tea catechin with potential health benefits and therapeutic effects in non-alcoholic fatty liver disease (NAFLD), a common liver disorder that adversely affects liver function and lipid metabolism. This systematic review surveyed the effects of EGCG or green tea extract (GTE) on NAFLD reported in studies involving rodent models or humans with a focus on clinicopathologic outcomes, lipid and carbohydrate metabolism, and inflammatory, oxidative stress, and liver injury markers. Articles involving clinical efficacy of EGCG/GTE on human subjects and rodent models were gathered by searching the PUBMED database and by referencing additional articles identified from other literature reviews. EGCG or GTE supplementation reduced body weight, adipose tissue deposits, and food intake. Mechanistically, the majority of these studies confirmed that EGCG or GTE supplementation plays a significant role in regulating lipid and glucose metabolism and expression of genes involved in lipid synthesis. Importantly, EGCG and GTE supplementation were shown to have beneficial effects on oxidative stress-related pathways that activate pro-inflammatory responses, leading to liver damage. In conclusion, green tea catechins are a potentially useful treatment option for NAFLD. More research is required to determine the ideal dosage, treatment duration, and most effective delivery method of EGCG or GTE, and to provide more definitive conclusions by performing large, randomized clinical trials.

Keywords: epigallocatechin-3-gallate; green tea extracts; non-alcoholic fatty liver disease.

Figure 1

PRISMA flow chart for murine studies, indicating how the 30 studies were chosen.

Figure 2

PRISMA flow chart for human studies indicating how the 21 studies were chosen.

Figure 3

EGCG-induced SIRT-1 modulation of lipid metabolism, antioxidant pathways, inhibition of fatty acid synthesis, and inflammatory response pathways. ATGL increases lipolysis of fats, while increased CAT boosts the antioxidant status. NF-kB regulates several pro-inflammatory pathways, including the production of inflammatory cytokines such as IL-6 and TNFα. Abbreviations: ATGL: adipose triglyceride lipase; CAT: catalase; FOXO-1: fork-head box O1; IL: interleukin; NF-κB: nuclear factor-κB; PGC: peroxisome proliferator-activated receptor-gamma coactivator; PPAR: peroxisome proliferator receptor; SREBP: sterol regulatory element binding protein; TNF: tumor necrosis factor.

Figure 4

Oxidative stress and antioxidation pathways. Gray boxes represent pro-oxidation end-products. Brown boxes represent pro-oxidation molecules. Yellow boxes represent antioxidation molecules. Reducing the production of H₂O₂ or increasing its breakdown will reduce the oxidant stress. EGCG appears to act via both mechanisms. The end result is reduced oxidative damage, as is evidenced by the reduced levels of MDA and 8-OHdG. Abbreviations: 8-OHdG: 8-hydroxy-2’-deoxyguanosine; CAT: catalase; CYP2E1: cytochrome-2E1; GSH: glutathione; MDA: malondialdehyde; ROS: reactive oxidative species; SOD: superoxide dismutase.