Effects of castration on the adiposity and expression of lipid metabolism genes in various fat depots of Korean cattle

Abstract

Castration increases intramuscular (IM) fat deposition in the musculus longissimus dorsi, a highly desirable trait in Korean beef cattle. However, castration may also affect accumulation in other fat depots. We examined whether castration affects adipose cellularity and lipid metabolism gene expression in various fat depots, including subcutaneous (SC), abdominal (AB), perirenal (PR), and IM fat. First, frozen sections taken from fat depots were stained with hematoxylin and eosin and the mean fat cell size was determined. Steers showed larger cell sizes in AB (P=0.01), SC (P=0.05), and PR (P=0.01) fat compared to bulls. Next, lipid metabolism gene expression in AB fat was compared between bulls and steers. In AB fat, steers showed increased mRNA expression of CCAAT/enhancer binding protein alpha (C/EBPα), a gene related to adipogenesis, compared to bulls (P<0.01). In contrast, steers showed decreased protein expression of medium-chain acyl-CoA dehydrogenase (MCAD), an enzyme involved in fatty acid β-oxidation, compared to bulls (P<0.05). Our results demonstrate that castration induces hypertrophy in body fat cells, and that the up-regulation of adipogenesis and down-regulation of fatty acid β-oxidation may in part contribute to this effect. We compared fat cell sizes among the various fat depots in Korean cattle steers. The order of fat cell size was AB>PR>SC>IM. The expression levels of lipid metabolism genes were compared among various fat depots. The mRNA levels of C/EBPα and peroxisome proliferator-activated receptor-γ were highest (P<0.05) in AB fat and lowest in IM fat. The mRNA levels of fatty acid binding protein-4 and lipogenic acetyl-coenzyme A carboxylase and fatty acid synthase genes were highest (P<0.05) in AB fat, and lowest in IM fat. Expression levels of lipolytic hormone-sensitive lipase and fatty oxidation MCAD genes were also highest (P<0.05) in AB fat and lowest in IM fat. Our results suggest that combined effects of higher adipogenesis, lipogenesis, and cellular fatty acid transport are responsible for the largest AB and smallest IM fat cells among the fat depots examined.