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Nutrient-Gene Interactions

Starvation and Feeding a High-Carbohydrate, Low-Fat Diet Regulate the Expression Sterol Regulatory Element-Binding Protein-1 in Chickens¹

Department of Biochemistry and Molecular Pharmacology, School of Medicine, West Virginia University, Morgantown, WV 265061

²To whom correspondence should be addressed. E-mail: fbhillgartner{at}hsc.wvu.edu.

In mammalian liver, the mature form of sterol regulatory element-binding protein-1c (SREBP-1c) is an important activator of a wide array of genes involved in triacylglycerol biosynthesis. Starvation and feeding a high-carbohydrate, low-fat diet modulate the concentration of mature SREBP-1c primarily by a pretranslational mechanism. It is not known whether alterations in nutritional status regulate the concentration of SREBPs in nonmammalian species. 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. Feeding a high-carbohydrate, low-fat diet also increased the concentration of precursor SREBP-1 and SREBP-1 messenger RNA in chick liver; however, the magnitude of this effect was substantially lower than that observed for mature SREBP-1. DNA binding experiments demonstrated that 3 protein complexes containing SREBP bound the acetyl-CoA carboxylase- (ACC) sterol regulatory element (SRE) in chick liver and that the binding activity of 2 of these complexes was increased by consumption of a high-carbohydrate, low-fat diet. Additional analyses showed that feeding a high-carbohydrate, low-fat diet had no effect on the concentration of mature SREBP-2 and the binding of SREBP-2 to the ACC SRE in chick liver. These results indicate that alterations in the concentration of mature SREBP-1 play a role in mediating the effects of starvation and feeding a high-carbohydrate, low-fat diet on ACC transcription in chick liver and that diet-induced changes in mature SREBP-1 concentration in chick liver are mediated primarily by a posttranslational mechanism.

KEY WORDS: • transcription • fatty acid synthesis • acetyl-CoA carboxylase • insulin • thyroid hormone

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