Effects of castration on expression of lipid metabolism genes in the liver of korean cattle

Abstract

Castration induces the accumulation of body fat and deposition of intramuscular fat in Korean cattle, resulting in improved beef quality. However, little is known about the metabolic adaptations in the liver following castration. To understand changes in lipid metabolism following castration, hepatic expression levels of lipid metabolism genes were compared between Korean bulls and steers. Steers had higher (p<0.001) hepatic lipids contents and higher (p<0.01) mRNA levels of lipogenic acetyl-CoA carboxylase. This differential gene expression may, in part, contribute to increased hepatic lipid content following the castration of bulls. However, we found no differences in the hepatic expression levels of genes related to triglyceride synthesis (mitochondrial glycerol-3-phosphate acyltransferase, diacylglycerol O-acyltransferase 1 and 2) and fatty acid (FA) oxidation (carnitine palmitoyltransferase 1A, C-4 to C-12 straight chain acyl-CoA dehydrogenase, very long chain acyl-CoA dehydrogenase) between bulls and steers. No differences in gene expression for very-low-density lipoprotein (VLDL) secretion, including apolipoprotein B mRNA and microsomal triglyceride transfer protein (MTTP) protein, were observed in the liver although MTTP mRNA levels were higher in steers compared to bulls. In conclusion, FA synthesis may contribute to increased hepatic lipid deposition in steers following castration. However, hepatic lipid metabolism, including triglyceride synthesis, FA oxidation, and VLDL secretion, was not significantly altered by castration. Our results suggest that hepatic lipid metabolism does not significantly contribute to increased body fat deposition in steers following castration.

Keywords: Bulls; Gene Expression; Korean Cattle; Liver; Steers.

Figure 1

Comparison of mRNA levels of fatty acid uptake and transporter genes between bulls and steers in the liver. mRNA levels were determined by real-time polymerase chain reaction, and results were normalized with the ribosomal protein S9 gene (n = 10). Values of bulls were normalized as 1.0. Values are shown as means+standard error of the means. * p<0.05; ** p<0.01. CD36, CD36 molecule; FATP5, fatty acid transporter 5; LPL, lipoprotein lipase.

Figure 2

Comparison of mRNA and protein levels of adipogenic (A), lipogenic (B), triglyceride (TG) synthesis (C), and cholesterol synthesis (D) genes between bulls and steers in the liver. mRNA levels were determined by real-time polymerase chain reaction, and the results were normalized with the ribosomal protein S9 gene (n = 10). Values of bulls were normalized as 1.0. Values are shown as means+standard error of the means. * p<0.05, ** p<0.01. SREBF1, sterol regulatory element binding transcription factor 1; RXRα, retinoid X receptor-alpha; RXRβ, retinoid X receptor-beta; RXRγ, retinoid X receptor-gamma; FASN, fatty acid synthase; ACC, acetyl-CoA carboxylase α; GPAM, glycerol-3-phosphate acyltransferase; DGAT1, diacylglycerol O-acyltransferase 1; DGAT2, diacylglycerol O-acyltransferase 2; LXRα, liver X receptor-alpha; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase.

Figure 3

Comparison of expression levels of fatty acid oxidation (A) and very-low-density lipoprotein (VLDL) secretion genes (B) genes between bulls and steers in the liver. mRNA levels were determined by real-time polymerase chain reaction, and they were normalized with the ribosomal protein S9 gene (n = 10). Protein levels (n = 4) were determined by Western blot analysis and normalized to β-actin levels. Values of bulls were normalized as 1.0. Values are shown as means+standard error of the means. * p<0.05. CPT-1a, carnitine palmitoyltransferase 1A (liver); ACADVL, acyl-CoA dehydrogenase very long chain; ACADM, acyl-CoA dehydrogenase, C-4 to C-12 straight chain; ApoB, apolipoprotein B; MTTP, microsomal triglyceride transfer protein.