Effects Of Glucocorticoids And Heat Stress On The Liver Lipid Metabolism Of Laying Hens

The effects of glucocorticoids (corticosterone) and heat stress on lipid metabolism were studied in vivo in laying hens. We focus on whether the stress would result in altered de novo synthesis and VLDL assembly in liver, leading to the liver lipid accumulation and lower production rate due to alter the York precursor.Trial 1 Hy-line brown laying hens (26 wk old, n=24) were raised when the room temperatrue was 31.0℃(±0.5) or 24℃for 1 wk. The blood and liver sample were obtained in th fasted status. Heat treatment significantly decreased the absolute weight of liver and abdominal fat in the fasting status (p<0.05). The content of liver TG had no change in heat-treated group. The heat stress had no effect on the liver lipogenic genes fatty acid synthase (FAS), acetyl-COA carboxylase (ACC), the stearoyl-COA desaturase (SCD), malic enzymes (ME) mRNA level and the transcription of lipogenic genes sterol-regulatory-element-binding protein 1c (SREBP-1C) , liver X-activated receptor (LXR) mRNA level(P>0.05). Two important genes of very low density Apolipoprotein (VLDL) assembly process apolipoprotein B (APOB) and very low density Apolipoprotein II (APOVLDL-II) mRNA expression had also no change in exposed high temperature laying hens (P>0.05). Only microsomal triglyceride transfer protein (MTP) mRNA lever were up-regulated in heat stress group in mini fasting status (P<0.01). The glucocorticoids receptor mRNA lever had no difference in heat stress group, which indicated that the heat stress had a tend to increased the APOB secret. These results suggested that the effect of heat stress on the relative genes of lipid metabolism may be not regulated by the GR.We can presume that the heat stress may be effect the laying production, laying rate, relative weight of yolk and so on, which may be the main way of by decreacing feed intake.Trial 2 Hy-line brown laying hens (26 wk old, n=24) were injected with CORT (corticosterone) (2mg/kg weight) or Corn oil (same dosage) for 1 wk. CORT administration resulted in enhanced lipid deposition in liver and increased the absolute weight of liver (P<0.01). By the HE staining on the hepatic tissue, showed that the Hepatocytes cytoplasmic vacuolation, Cell Nucleus shifting and deformation, due to the accumulation of large amounts of lipid in CORT-treated laying hens. In CORT injected laying hens, increased significantly liver lipogenic genes fatty acid synthase (FAS), acetyl-COA carboxylase (ACC), malic enzymes (ME) and stearoyl-COA desaturase (SCD1) mRNA level and the transcription of lipogenic genes sterol-regulatory-element-binding protein 1c (SREBP-1C) mRNA level was also significantly up-regulated (P<0.05). Two important genes of York-targeted VLDL (VLDLY) assembly process apolipoprotein B (APOB) and very low density Apolipoprotein II (APOVLDL-II) were decreased in mini fasting status (P<0.01). In the feeding state, significantly up-regulated fatty acid synthase (FAS) mRNA expression, but no change on acetyl-COA carboxylase (ACC), malic enzymes (ME) and stearoyl-COA desaturase (SCD1) mRNA expression in CORT-treated laying hens. CORT administration resulted in significantly down-regulated apolipoprotein B (APOB) and very low density Apolipoprotein II (APOVLDL-II) mRNA expression in feeding state (p<0.05). These results showed that the CORT induce the stress response and affect the liver function and liver lipid metabolism. The results indicated that the increased hepatic de novo lipogenesis and decreased VLDLY assemble process contributes to the augmented fat deposition in liver tissues and decreased circulating lipid filux and York precursor VLDL concentration in CORT-treated laying hens.Trial 3 Hy-line brown laying pullets (14 wk old, n=32) and Roosters (10 wk old, n=32) were selected, were randomly assigned to four groups of eight birds each: vehicle, estrogen, CORT or estrogen plus CORT. The experence priod was 7days. The result showed that the CORT and ES both increased the relative weight of liver in laying pulltes and Rooster(P<0.01). ES administrition had significantly increased the plasma triglyceride (TG), non-esterified fatty acid (NEFA), very low density lipoprotein (VLDL) and calcium (GA), phosphorus (P) concentration (P<0.01). ES or CORT administrition had significantly decreased the liver CPT activities (P<0.01). CORT had significantly up-regulated the expression of relative lipid metabolism genes fatty acid synthase (FAS), acetyl-COA carboxylase (ACC) and the stearoyl-COA desaturase (SCD) mRNA level in liver (P<0.01).But ES had down-regulated the FAS mRNA (P<0.05)and up-regulated SCD1 mRNA level (P<0.01) in rooster.The two factors has an interaction in the effect on lipid metabolism, but has an divergent effect on the expression of apob100 and apovldl-‖mRNA. Some results showed that the cort and ES demage the liver and kindey fuction and affect the lipid metabolism. The results indicate that GC inhibit the effect of ES on the VLDL secret should be responsible for the fat deposition in liver.Trial 4 Hepatocytes were isolated from livers of 14 days Chick Embryo. Cells were incubated in williams'medium E containing 10% serum. Cell trial1: After 48 h incubation, there were four treatments, one of which had the same composition supplemented with DEX (200nmol/L), ES (50nmol/L) or both. The control group contained neither of the hormones. Cell trial2: After 48 h incubation, there were four treatments, one of which had the same composition supplemented with DEX (200nmol/L), INS (100nmol/L) or both. Afer 24h of treatment, total RNA was isolated and the expression of relative lipid metaboliasm genes were measured by real-time PCR. The cell trial 1 results found that DEX decreased significantly ACC and SREBP-1C mRNA level (P<0.01), but had no effect on FAS mRNA level(P>0.05). DEX and ES down-regulted LXRαmRNA level (P<0.01). The cell trial 2 results found that DEX decreased significantly ACC and LXR mRNA level (P<0.01), ES decreased the SREBP-1C mRNA level(P<0.05), but had no effect on the ACC, FAS, LXR and APOB100 mRNA level(P>0.05). These results suggested that DEX and ES both decreased de novo lipogenesis in chick embryo. The transcription of lipogenic genes perhaps were modulated by LXRαand/or SREBP-1. Which was not agree with the vivo.