*4.2.2 Tea consumption and NAFLD*

Tea intake modulates NAFLD by suppressing inflammation and lipogenesis while promoting fatty acid β-oxidation. *Camellia sinensis* leaves and buds are used to make green and black tea, however, due to variations in post-harvest processing, their polyphenol content varies. Catechins (flavan-3-ols), which make up about 20% of the total flavonoids in green tea leaves are the main polyphenols and EGCG (Epigallocatechin gallate) [2, 22]. In humans, between the ages of 10 and 16, drinking green tea has been shown to lower plasma levels of aminotransferases, triglycerides, and improve BMI, explaining that drinking tea helps protect against NAFLD is supported by the tight association between these factors and NAFLD. *In-vivo* research has previously demonstrated that green tea has antioxidant capabilities, it reduces the accumulation of lipids in the liver and adipose tissue and prevents intestinal absorption of dietary lipids. In the mouse model of NAFLD, green tea extract (GTE) has been discovered to protect against hepatic steatosis and related liver damage. Recent research suggests that GTE therapy reduces pro-inflammatory signals through TLR4 and TNFR1, which in turn reduces inflammation in steatohepatitis [22]. Green tea catechins have also been demonstrated to support hepatic lipid metabolism. It was suggested that oxidative degradation of fatty acids by catechins acts as a protective mechanism against NAFLD and also functioning as a natural iron chelator. It has been found that giving patients EGCG reduces non-heme iron absorption by 27%. Since elevated hepatic iron levels have been linked to NASH in patients, while catechins that block iron absorption may be a useful treatment for NAFLD. Similar to this, theaflavin from black tea reduced liver steatosis, oxidative stress, inflammation, and apoptosis in mice with NAFLD-induced ischemia-reperfusion injury [22].
