It has been known that the changes in gonadal steroids are closely associated with adipose tissue metabolism. Domestic pigs have been a well-recognized experimental animal in biomedical research because of their similarity to humans in body size and other physiological/anatomical features. The aims of this study were to investigate the influence of castration-induced sex hormone deficiency on serum lipid levels and the genes expression of key enzymes associated with lipogenic and lipolytic processes in male pigs. The experimental animals consisted of 2 groups slaughtered on 147th and 210th day, respectively. In each of the group, 7 full-sib pairs of castrated and intact male hybrids from Yorkshire dams sired by Landrace were contained. The results showed that castration of male pigs led to increased total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, and leptin levels in serum (p<0.05). No differences in levels of the free fatty acid, insulin, and glucose were observed between boars and barrows (p>0.05). Castration caused upregulation of fatty acid synthase and acetyl-CoA carboxylase alpha genes expression at both 147 and 210 days of age (p<0.05). No differences in expression of hormone sensitive lipase and adipose tissue triglyceride lipase genes were observed between boars and barrows at either 147 or 210 days of age (p>0.05). It is speculated that higher body fat deposition in castrated male pigs might have resulted mainly from increased transcription of the lipogenic genes, but not from decreased transcription of the lipolytic genes.

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Lipoprotein lipase (LPL), which consists of an N-terminal catalytic domain and a C-terminal binding domain, is a crucial enzyme in the metabolism of lipids. Binding in the presence of cofactors or receptors on the cell surface, LPL catalyses the hydrolysis of triglycerides in the lipoprotein. To investigate the correlation between the LPL gene and adipose traits, single nucleotide polymorphisms in the exons of LPL in two breeds, Tibet chicken and E-white recessive rock (EWRR) chicken were investigated. The two breeds have significantly different levels of obesity. They were screened with single-strand conformation polymorphism and its effect on adipose traits was analysed. The results showed that a missense mutation G–C in the seventh exon of LPL changed alanine 377 to proline at the C-terminal binding domain, which is involved in the binding activity of LPL. Association analysis showed that the intermuscular adipose tissue width of Tibet chicken with the CC genotype decreased significantly (P < 0.05), while abdominal adipose weight of EWRR chicken of the CC genotype increased markedly (P < 0.05) compared with the individuals of other genotypes. Although the mutation correlated with very low-density lipoprotein in Tibet chicken, it did not demonstrate significant association with the lipoprotein in EWRR chicken (P > 0.05). Neither the glucose or triglyceride levels of chickens with different genotypes differed significantly (P > 0.05). As very low-density lipoprotein content and fat mass were upregulated by LPL, we concluded that the A377P mutation may enhance the binding activity of the LPL C-terminal domain to very low-density lipoprotein receptors, which promoted triglyceride metabolism in very low-density lipoprotein.