Loss of TRIM67 Attenuates the Progress of Obesity-Induced Non-Alcoholic Fatty Liver Disease

Obesity is considered as a major cause for the development and progress of non-alcoholic fatty liver disease (NAFLD), which is one of the most prevalent chronic liver diseases worldwide. However, molecular mechanisms that implicate in obesity-driven pathophysiology of NAFLD are not well defined. Here, we report a tripartite motif (TRIM) protein family member-TRIM67-that is hardly expressed in liver but is inducible on obese conditions. Enhanced expression of TRIM67 activates hepatic inflammation to disturb lipid metabolic homeostasis and promote the progress of NAFLD induced by obesity, while the deficiency in TRIM67 is protective against these pathophysiological processes. Finally, we show that the important transcription coactivator PGC-1 alpha implicates in the response of hepatic TRIM67 to obesity.

Automated summary

Obesity is a major factor in the development and progression of non-alcoholic fatty liver disease (NAFLD), but the molecular mechanisms involved are not well understood. This study investigates the role of TRIM67, a protein that is induced under obesity conditions, in NAFLD pathophysiology. It is found that enhanced expression of TRIM67 leads to hepatic inflammation, disruption of lipid metabolic homeostasis, and promotion of NAFLD progression induced by obesity. Furthermore, the transcription coactivator PGC-1 alpha is implicated in the response of hepatic TRIM67 to obesity.