Dietary fatty acids and the regulation of gene expression

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In bacteria or unicellular eukaryotic cells, fatty acids (FAs) display their dual role of structural membrane components and suppliers of energy. Supply of FAs leads to the down-regulation of endogenous FA synthesis and to the up-regulation of genes coding for transport and metabolism of FAs. This is a sparing process that is achieved through the binding of acyl-CoA to a specific DNA binding protein that changes its affinity for DNA response elements. In mammals, the expression of genes involved in transport and metabolism appears to be regulated by FAs in a positive or a negative manner. However, the simple bacterial process could provide the paradigm of the regulation of gene expression by FAs. FAs or derivatives depress genes coding for enzymes involved in lipogenesis and activate those that allow the transport and the oxidation of FAs. FA binding to transcription factors modifies their involvement in the transcription process. As a matter of fact, in mammals several genes coding for proteins involved in lipogenesis or weight control such as leptin, are down-regulated. This mechanism may be related to the decrease in hepatic de novo lipogenesis that can be observed in animals and humans submitted to a polyunsaturated fatty acid (PUFA)-rich diet. In contrast, other genes are up-regulated, such as those coding for proteins involved in transport and oxidation of FA (FAT-CD36, LPL, FABPs, CPT 1). Some other genes are regulated in a tissue-specific way, for example, PEP-CK is up-regulated in adipocytes but not in the liver (Antrasferry et al., 1994).

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