Association analyses of a SNP in the promoter of IGF1 with fat deposition and carcass merit traits in hybrid, Angus and Charolais beef cattle.

A SNP in the promoter region of insulin like growth factor-1 (IGF1) (c.-512C>T) was analysed for associations with 10 fat deposition and carcass merit traits in hybrid (n = 455), Angus (n = 204) and Charolais (n = 186) beef cattle populations. Significant associations of the SNP were found for ultrasound backfat thickness (P = 0.030), carcass average backfat (P = 0.015) and carcass lean meat yield (LMY) (P = 0.023) in the Angus beef population, with the 'CC' genotype showing higher fat depth and lower LMY than the 'TT' genotype. Analyses of transcription factor binding sites based on transcription element search system prediction revealed that the 'C' allele introduces a binding site for nuclear factor I, which has an adipose tissue-specific regulatory role and thus may contribute to the SNP effect on fat deposition in the population of pure Angus cattle, a breed with greater fat depth than the hybrid and Charolais breeds.

Deficiency of PPARalpha disturbs the response of lipogenic flux and of lipogenic and cholesterogenic gene expression to dietary cholesterol in mouse white adipose tissue.

PPARalpha-deficiency in mice fed a high-carbohydrate, low-cholesterol diet was associated with a decreased weight of epididymal adipose tissue and an increased concentration of adipose tissue cholesterol. Consumption of a high (2% w/w) cholesterol diet resulted in a further increase in the concentration of cholesterol and a further decrease in epididymal fat pad weight in PPARalpha-null mice, but had no effect in the wild-type. These reductions in fat pad weight were associated with an increase in hepatic triacylglycerol content, indicating that both PPARalpha-deficiency and cholesterol altered the distribution of triacylglycerol in the body. Adipose tissue de novo lipogenesis was increased in PPARalpha-null mice and was further enhanced when they were fed a cholesterol-rich diet; no such effect was observed in the wild-type mice. The increased lipogenesis in the chow-fed PPARalpha-null mice was accompanied paradoxically by lower mRNA expression of SREBP-1c and its target genes, acetyl-CoA carboxylase and fatty acid synthase. Consumption of a high-cholesterol diet increased the mRNA expression of these genes in the PPARalpha-deficient mice but not in the wild-type. De novo cholesterol synthesis was not detectable in the adipose tissue of either genotype despite a relatively high expression of the mRNA's encoding SREBP-2 and 3-hydroxy-3-methylglutaryl Coenzyme A reductase. The mRNA expression of these genes and of the LDL-receptor in adipose tissue of the PPARalpha-deficient mice was lower than that of the wild-type and was not downregulated by cholesterol feeding. The results suggest that PPARalpha plays a role in adipose tissue cholesterol and triacylglycerol homeostasis and prevents cholesterol-mediated changes in de novo lipogenesis.