Research Progress on Leptin in Metabolic Dysfunction-associated Fatty Liver Disease.

Area of Science:

• Hepatology
• Endocrinology
• Metabolic Syndrome

Background:

• Metabolic dysfunction-associated fatty liver disease (MAFLD) is a prevalent condition with complex pathogenesis.
• MAFLD involves hepatocyte triglyceride accumulation, insulin resistance, inflammation, and oxidative stress.
• Leptin's liver functions, both direct and CNS-mediated, are crucial in metabolic regulation.

Purpose of the Study:

• To review leptin's structure and physiological functions.
• To explore leptin's multifaceted role in the pathogenesis of MAFLD.
• To evaluate leptin as a potential therapeutic target for MAFLD.

Main Methods:

• Literature review of studies on leptin, MAFLD, and related metabolic pathways.
• Analysis of leptin's effects on hepatic glucose and lipid metabolism.
• Examination of leptin's influence on fibrogenesis and inflammatory responses in the liver.

Main Results:

• Leptin improves glucose metabolism via enhanced insulin sensitivity.
• Leptin regulates lipid metabolism by promoting oxidation and export, inhibiting synthesis.
• Leptin may contribute to fibrogenesis by upregulating TGF-β and activating HSCs and immune cells.

Conclusions:

• Leptin exerts significant regulatory effects on hepatic glucose and lipid homeostasis.
• Leptin's dual role in MAFLD pathogenesis, affecting metabolism and fibrogenesis, is highlighted.
• Targeting leptin pathways presents a promising therapeutic strategy for managing MAFLD.