High impact information on SREBF1

• These results indicate that SREBP-1 directly interacts with TR-retinoid X receptor in an orientation-specific manner to enhance T3-induced ACCalpha transcription in hepatocytes [1].
• SREBP-1 integrates the actions of thyroid hormone, insulin, cAMP, and medium-chain fatty acids on ACCalpha transcription in hepatocytes [2].
• Treatment with cAMP or hexanoate suppresses the increase in mature SREBP-1 abundance caused by T3 and insulin [2].
• In chick embryo hepatocytes, activation of acetyl-CoA carboxylase-alpha (ACCalpha) transcription by 3,5,3'-triiodothyronine (T3) is mediated by a cis-acting regulatory unit (-101 to -71 bp) that binds the nuclear T3 receptor (TR) and sterol regulatory element-binding protein-1 (SREBP-1) [2].
• Moreover, overexpression of ADD-1/SREBP-1 by adenoviral gene transfer induces FAS in chicken adipocytes, where lipogenesis is normally low [3].

Biological context of SREBF1

• Genetic linkage and expression analysis of SREBP and lipogenic genes in fat and lean chicken [4].
• These changes were accompanied by a significant down-regulation of leptin receptor gene expression, however SREBP-1, the main transcription factor of lipogenic genes, remained unchanged [5].

Analytical, diagnostic and therapeutic context of SREBF1

• In this study, we found that in previously starved chicks, feeding a high-carbohydrate, low-fat diet stimulated a robust increase (14-fold at 5 h of feeding) in the concentration of mature SREBP-1 in liver [6].

References