The Molecular Mechanisms Of Lipid Deposition In Stressed Broiler Chickens | | Posted on:2010-02-07 | Degree:Doctor | Type:Dissertation | | Country:China | Candidate:Y L Cai | Full Text:PDF | | GTID:1103360278967388 | Subject:Animal breeding and genetics and breeding | | Abstract/Summary: | PDF Full Text Request | | The effects of dexamethasone on lipid metabolism were studied in vivo and in primary culture of hepatocytes in broiler chickens.Effect of dexamethasone (DEX, a synthetic glucocorticoid) on lipid metabolism in broiler chickens (Gallus gallus domesticus) was investigated in the early growing stage. Male Arbor Acres chickens (1 wk old, n=30) were injected with DEX or saline for 1 wk, and a pair-fed group was included. DEX administration resulted in enhanced lipid deposition in adipose tissues. Plasma insulin increased about 3.3 fold in DEX injected chickens as against the control and hepatic triglyceride was higher as compared with the pair-fed chickens. In DEX injected chickens, the hepatic activities of malic enzyme (ME) and fatty acid synthetase (FAS) was significantly increased, while the mRNA levels of acetyl CoA carboxylase (ACC), ME, and FAS was significantly up-regulated, compared with the control. Although the mRNA levels of lipoprotein lipase (LPL), peroxisome proliferator-activated11 receptor-γ(PPARγ) and adipose triglyceride lipase (ATGL) genes in adipose tissue were not affected by DEX injection, ME activity and mRNA levels in abdominal fat pad of chickens treated with DEX is higher than those of control chickens. The results indicated that the increased hepatic de novo lipogenesis and in turn, the increased circulating lipid flux contributes to the augmented fat deposition in adipose tissues and liver in DEX-challenged chickens. The results suggest that glucocorticoids together with the induced hyperinsulinemia should be responsible for the up-regulated hepatic lipogenesis.Effects of DEX on lipid metabolism in broiler chickens (Gallus gallus domesticus) were investigated in the late growing stage. Male Arbor Acres chickens (35 d of age, n=30) were injected with DEX or saline for 3d, and a pair-fed group was included. When the samples were collected at 38 d of age, one half of chickens were in the fed status, another half were fasted for 12h. DEX administration resulted in enhanced lipid deposition in cervical fat, abdomnal fat and thigh fat also had increased trend. DEX injection increased plasma TG, VLDL and insulin concentration not only in fasted status but also in fed status. DEX administration led to higher post-heparin LPL activity and plasma glucose level in fasted status. In fasted status, DEX administration resulted in increased ME activity in liver, liver FAS activity tended to increase in DEX injected chicken. But the FAS and ME activity in DEX chickens had no significant change in fed status. DEX injection resulted in enhanced ACC and FAS mRNA levels in liver in fasted status. Compared to pair-fed, ME mRNA level in liver tended to increase in DEX chickens in fasted status. In fed status, DEX administration led to enhanced liver ACC and ME mRNA expressions compared to pair-fed chickens. DEX administration up-regulated FAS mRNA expression in abdominal fat in fasted status, but the ME and FAS mRNA levels of abdominal fat in fed status were not altered by DEX injection. DEX injection resulted in LPL mRNA expression of abdominal fat in fed status, and in fasted status LPL mRNA level trended to increase by DEX injection. We also measured the mRNA levels of PPARγand ATGL in abdominal fat in fasted and fed status. Neither of these two genes'mRNA expression was altered by DEX injection. The results suggested that the increased hepatic de novo lipogenesis and in turn, the increased circulating lipid flux contributes to the augmented fat deposition in adipose tissues in DEX-challenged chickens which agreed to the former experiments. Up-regulation of LPL mRNA level in abdominal fat and increased plasma LPL activity also contribute to the enhanced fat deposits which were not accordant with results in the early growing stage of chickens perhaps because of more abdominal fat deposit. The results indicated that glucocorticoids together with the induced hyperinsulinemia should be responsible for the up-regulated hepatic lipogenesis.The effects of DEX and insulin on the fatty acid synthesis of hepatocytes cultured in vitro were investigated in the third experiment. Hepatocytes were isolated from livers of 6 day old chick. Cells were incubated in Williams'Medium E containing 10% serum. After 15 h incubation, the medium was changed to contain 5% serum. There were four treatments, one of which had the same composition supplemented with DEX (200nmol/L), insulin (100nmol/L) or both. The control group contained neither of the hormones. Afer 24h of treatment, total RNA was isolated and lipogenic genes were measured by real-time PCR. The results found that in combination with DEX, insulin increased significantly FAS, ACC and ME mRNA level, but when added alone, DEX or insulin had no effent on these lipogenic genes. The effects of the two hormones on nucleus transcriptional factors were also evaluated. DEX and insulin synergically promoted LXRαmRNA level. When DEX plus insulin were added to the medium, SREBP-1c tended to increase compared to DEX or control group. The results suggested that it was insulin plus DEX that enhanced hepatic de novo lipogenesis. The transcription of lipogenic genes perhaps were modulated by LXRαand/or SREBP-1. | | Keywords/Search Tags: | stress, Dexamethasone, insulin, fat deposition, de novo lipogenesis, gene expression | PDF Full Text Request | Related items |
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