While metabolic syndrome and alcohol consumption are the two main causes of chronic liver disease, one of the two conditions is often predominant, with the other acting as a cofactor of morbimortality. It has been shown that obesity and alcohol act synergistically to increase the risk of fibrosis progression, hepatic carcinogenesis and mortality, while genetic polymorphisms can strongly influence disease progression. Based on common pathogenic pathways, there are several potential targets that could be used to treat both diseases; based on the prevalence and incidence of these diseases, new therapies and clinical trials are needed urgently.
Keywords: ACC, acetyl-CoA carboxylase; ALD; ALD, alcohol-related liver disease; ASH; ASH, alcohol-related steatohepatitis; ASK-1, apoptosis signal-regulating kinase 1; Alcohol; BMI, body mass index; CLD, chronic liver disease; CPT, carnitine palmitoyltransferase; DNL, de novo lipogenesis; EASL, European Association for the Study of the Liver; ER, endoplasmic reticulum; FXR, farnesoid X receptor; HCC, hepatocellular carcinoma; HSD17B13, hydroxysteroid 17-beta dehydrogenase 13; IL, interleukin; LPS, lipopolysaccharide; MBOAT7, membrane bound O-acyl transferase 7; MELD, model for end-stage liver disease; NAFLD; NAFLD, non-alcoholic fatty liver disease; NASH; NASH, non-alcoholic steatohepatitis; OR, odds ratio; PAMP, pathogen-associated molecular pattern; PI3K, phosphatidylinositol-3-kinase; PIP3, phosphatidylinositol 3,4,5-triphosphate; PNPLA3, palatin-like phospholipase domain-containing 3; PRKCE, protein kinase C Epsilon; ROS, reactive oxygen species; SREBP-1c, sterol regulatory element binding protein-1c; TLR, Toll-like receptor; TM6SF2, transmembrane 6 superfamily member 2; TNF-α, tumour necrosis factor-α; WHO, World Health Organization; diabetes; metabolic syndrome; obesity.
© 2020 The Authors.