Published online May 15, 2023. doi: 10.4239/wjd.v14.i5.549
Peer-review started: December 3, 2022
First decision: December 26, 2022
Revised: February 2, 2023
Accepted: April 11, 2023
Article in press: April 11, 2023
Published online: May 15, 2023
Processing time: 163 Days and 0.1 Hours
Fatty liver disease is defined as liver condition characterized by hepatic steatosis, closely related to pathological conditions in type 2 diabetes and obesity. The high prevalence of fatty liver disease in obese patients with type 2 diabetes reached 70%, reflecting the importance of these conditions with fatty liver. Although the exact pathological mechanism of fatty liver disease, specifically non-alcoholic fatty liver disease (NAFLD) remains not completely revealed, insulin resistance is suggested as the major mechanism that bridged the development of NAFLD. Indeed, loss of the incretin effect leads to insulin resistance. Since incretin is closely related to insulin resistance and the resistance of insulin associated with the development of fatty liver disease, this pathway suggested a potential me-chanism that explains the association between type 2 diabetes and NAFLD. Furthermore, recent studies indicated that NAFLD is associated with impaired glucagon-like peptide-1, resulting in decreased incretin effect. Nevertheless, improving the incretin effect becomes a reasonable approach to manage fatty liver disease. This review elucidates the involvement of incretin in fatty liver disease and recent studies of incretin as the management for fatty liver disease.
Core Tip: Type 2 diabetes mellitus (T2DM) is correlated with various metabolic disorders, including fatty liver. The influence of T2DM on incretin hormones contributed to fatty liver development. Impairment in lipid and glucose metabolism, fat oxidation, oxidative stress, and other effects lead to liver fat deposition. Therefore, drugs targeting the incretin hormones may provide beneficial effects on patients.
