Effect of castration and exogenous testosterone implantation on lipogenesis, lipid metabolism and lipid relevant hormones in male chickens

• Main Authors: Wen-Tzu Chi, 杞文慈
• Other Authors: Kuo-Lung Chen
• Format: Others
• Language: zh-TW
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/37948832239463464455

碩士 === 國立嘉義大學 === 動物科學系碩士班 === 92 === The purpose of this study is to investigate the castration and testosterone implantation level effects on growth, carcass characteristics and appearance, lipid synthesis, transport, metabolism and gene expression, and lipogenesis relevant hormones in male chickens, to reveal the role of testosterone in male chickens. The study was subdivided into 5 parts with two trials in each part of study. In all studies, healthy and uniform male Single Comb White Leghorn chickens were castrated at 12-weeks-old and selected at 16-weeks-old for a 10-week feeding experiment; Fifteen males and 15 castrated (capon) chickens were randomly allocated to trial 1, while 10 sham operation chickens (sham) and 40 capons (randomly divided into four treatments), which were implanted with cholesterol (1.62 mm i.d., 3.16 mm o.d., 9.24±0.36mg), low testosterone (1 mm i.d., 3 mm, o.d., 5.88±0.23mg), medium (1.62 mm i.d., 3.16 mm, o.d., 9.81±0.17mg) or high (2 mm i.d., 4 mm, o.d., 16.7±0.24mg) dose treatments, respectively, and were implanted at 16, 20 and 24-weeks-old in trial 2. First study was conducted to determine the effect on growth, appearance and carcass characteristics. Results showed that castration significantly increased (P < 0.05) body weight gain, gastrointestinal (GI) tract weight, breast weight and abdominal fat weight, and their relative weight, while significantly decreased (P < 0.05) male secondary sexual characteristics (comb length, height and weight) in capon, and did not significant influence (P > 0.05) body weight and feed intake in trial 1. High dose testosterone implantation inhibited abdominal fat accumulation with no significantly difference with sham (P > 0.05), improved the appearance characteristics, but did not reach the identical level in the sham (P < 0.05) in trial 2. The 2nd study was conducted to determine the cause of lipid accumulation after castration, whether is direct due to the androgen function or in coordinate with other hormones. Results showed that castration significantly decreased (P < 0.05) the blood testosterone (TES), growth (GH) and adrenocorticotrophic (ACTH) hormone concentrations, but did not significantly influence (P > 0.05) the blood estradiol (E2), triiodothyronine (T3) and insulin (INS) concentrations in trial 1; High dose testosterone implantation significantly increased (P < 0.05) blood TES concentration, which did not reach the identical level as in the sham (P > 0.05), and significantly decreased blood ACTH concentration than the sham (P < 0.05), however, did not significantly influenced (P > 0.05) blood E2, GH, T3 and INS concentrations in trial 2. The 3rd study was to investigate the effect on blood lipid, lipoprotein composition and structure in male chickens; Castration did not showed significantly influence on blood lipid composition (P > 0.05), showed trend (P = 0.08) toward increased triacylglycerol (TG), significantly increased (P < 0.05) low density lipoprotein (LDL) and high density lipoprotein (HDL) content, and protein (PRO) ratio in LDL and HDL, and significantly (P < 0.05) decreased LDL-free cholesterol (LDL-FC), HDL-FC and HDL-phospholipids (HDL-PL) ratios in trial 1; High dose testosterone implantation significantly increased glucose and glycerol concentrations, while medium dose testosterone implantation significantly increased non-esterifies fatty acid (NEFA) concentration compared to cholesterol implantation. cholesterol implanted capon on the other hand, showed significantly decreased LDL-PL and HDL-PL ratios (P < 0.05) and increased HDL-PRO ratio (P < 0.05) compared to the sham, however, TES implantation did not reach the identical level as in the sham in trial 2. The 4th study was conducted to determine the effects on the apolipoprotein (apo) composition within the lipoproteins. Results showed that castration did not significantly affect (P > 0.05) various apo ratios in LDL at 16, 21 and 26-weeks-old capon, but increased (P < 0.05) apo 66 kDa and decreased (P < 0.05) apo A-I in 26-weeks-old capons compared to male chickens. Testosterone implantation did not significantly influence (P > 0.05) apo ratios in LDL. In HDL, castration significantly increased apo 66 kDa and decreased apo A-I in HDL at 16-weeks-old and significantly increased apo 66 kDa (P < 0.05) and decreased apo C-like and E-like (P < 0.05) in HDL in 26-weeks-old as compared from CHOL implanted to the sham. TES implantation significantly decreased apo 66 kDa in HDL (P < 0.05), as shown in the high dose testosterone implanted exhibiting significantly lower than the CHOL implanted (P < 0.05). However, this was still significantly higher (P < 0.05) than that of the sham. All testosterone implanted capon and sham showed significantly lower (P < 0.05) apo C-like ratios in HDL compared to the CHOL implanted capon. The aim of 5th study was to determine the effects and role of testosterone on liver lipid composition, hepatic lipogenic enzyme activity and gene expression. Results showed that castration significantly increased (P < 0.05) the total hepatic lipid content and decreased (P < 0.05) the liver NEFA ratio, significantly increased (P < 0.05) in NADP-malic dehydrogenase (MDH) activity, and a trend (P = 0.095) toward increase in MDH mRNA content, but did not show significant influence (P > 0.05) in ATP-citrate cleavage enzyme (CCE), glucose-6-phosphate dehydrogenase (G-6-PDH), acetyl-CoA carboxylase (ACC) and fatty acid synthetase (FAS) in trial 1. Increase testosterone implantation dose significantly increased (P < 0.05) the liver NEFA ratio. TES implantation, however, did not significantly influence (P > 0.05) lipogenic enzyme activity including CCE, G-6-PDH, ACC and FAS, and high dose TES implantation showed a decrease trend toward MDH activity, but no significantly difference between the sham and the CHOL implantation. Castration significantly increased (P < 0.05) MDH activity, as shown in the CHOL group. Testosterone implantation did not affect MDH mRNA content (P > 0.05) in trial 2. It appears that castration decreases blood TES and ACTH concentrations, decreases lipogenic depression factor, lead to raise MDH activity, enhance liver lipogenesis. These effects increase blood TG content, change lipoprotein profile, alter apo ration in HDL, affect lipoprotein transport and therefore increases lipid accumulation. Testosterone implantation up to the threshold concentration depresses hepatic lipogenesis, changes lipoprotein transport and then decreases lipid accumulation.