利拉鲁肽
脂肪生成
FGF21型
生物信息学
疾病
肝病
医学
脂肪肝
酒精使用障碍
药理学
受体
2型糖尿病
内科学
糖尿病
内分泌学
生物
脂质代谢
酒
生物化学
成纤维细胞生长因子
作者
George Marek,Harmeet Malhi
标识
DOI:10.1097/hep.0000000000000935
摘要
New guidelines for the definitions of steatotic liver disease have named the entity of metabolic dysfunction and alcohol-associated liver disease (MetALD) as an overlap condition of metabolic dysfunction–associated steatotic liver disease (MASLD) and alcohol-associated liver disease. There is a broad range of therapeutics in all stages of development for MASLD, but these therapeutics, in general, have not been studied in patients with significant ongoing alcohol use. In this review, we discuss the current understanding of the endogenous and exogenous risks for MASLD and MetALD. Rational strategies for therapeutic intervention in MetALD include biopsychosocial interventions, alcohol use cessation strategies, including the use of medications for alcohol use disorder, and judicious use of therapeutics for steatotic liver disease. Therapeutics with promise for MetALD include incretin-based therapies, FGF21 agonists, thyroid hormone receptor beta agonists, sodium-glucose co-transporter 2 inhibitors, and agents to modify de novo lipogenesis. Currently, glucagon-like peptide 1 receptor agonists and peroxisome proliferator–activated receptor γ agonists have the largest body of literature supporting their use in MASLD, and there is a paucity of agents in trials for alcohol-associated liver disease. From existing studies, it is not clear if unique therapeutics or a combinatorial approach are needed for MetALD. Further elucidation of the safety and benefits of MASLD-related therapies is of paramount importance for advancing therapeutics for MetALD in carefully designed inclusive clinical trials.
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