Premium
Role of ChREBP in hepatic steatosis and insulin resistance
Author(s) -
Denechaud Pierre-Damien,
Dentin Renaud,
Girard Jean,
Postic Catherine
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.07.084
Subject(s) - carbohydrate responsive element binding protein , lipogenesis , insulin resistance , fatty liver , steatosis , medicine , endocrinology , fatty acid synthase , fatty acid synthesis , fatty acid , biology , insulin , chemistry , biochemistry , transcription factor , lipid metabolism , disease , gene
Non‐alcoholic fatty liver disease is tightly associated with insulin resistance, type 2 diabetes and obesity, but the molecular links between hepatic fat accumulation and insulin resistance are not fully identified. Excessive accumulation of triglycerides (TG) is one the main characteristics of non‐alcoholic fatty liver disease and fatty acids utilized for the synthesis of TG in liver are available from the plasma non‐esterified fatty acid pool but also from fatty acids newly synthesized through hepatic de novo lipogenesis. Recently, the transcription factor ChREBP (carbohydrate responsive element binding protein) has emerged as a central determinant of lipid synthesis in liver through its transcriptional control of key genes of the lipogenic pathway, including fatty acid synthase and acetyl CoA carboxylase. In this mini‐review, we will focus on the importance of ChREBP in the physiopathology of hepatic steatosis and insulin resistance by discussing the physiological and metabolic consequences of ChREBP knockdown in liver of ob/ob mice.