Effects of L-arginine supplementation on glucose and nitric oxide (NO) levels and activity of NO synthase in corticosterone-challenged broiler chickens (Gallus gallus).
ABSTRACT In the present study, three experiments were conducted to investigate the effect of oral supplementation of l-arginine (ARG) on the disposal of glucose in stressed-broiler chickens (Gallus gallus domesticus). In all the three experiments, the broiler chickens were randomly subjected to one of the four treatments at the beginning of the experiments: oral administration of saline, glucose (2.0g/kg body weight, BW), l-arginine (0.5g/kg BW) or mixed solution (2.0g glucose+0.5g arginine/kg BW). Immediately after the oral treatment, the experimental chickens were subcutaneously injected with corn oil (Experiment 1), corticosterone (CORT, 4mg/kg BW, Experiment 2) or insulin (1U/kg BW, Experiment 3), respectively. Blood samples were obtained at the beginning (0-h), 0.5-, 1- and 2-h time points after injection and the levels of plasma glucose, urate, nitric oxide (NO) and activity of NO synthase (NOS) were measured. The results showed that plasma NO levels and NOS activity were significantly suppressed while glucose and insulin concentrations were increased by CORT treatment. In contrast, insulin administration improved the circulating level of NO and activity of NOS. ARG supplementation could not improve the circulating levels of NO and NOS activity in CORT-challenged chickens and, in turn, the glucose disposal. The result suggests that NO is involved in insulin-mediated glucose transport in chickens, as well as that in mammals. The reduced circulating level of NO resulted from the suppressed activity of NOS rather than the reduced substrate concentration.
- [Show abstract] [Hide abstract]
ABSTRACT: This review discussed metabolism in poultry and wild birds with an emphasis on what remains to be elucidated. Circulating concentrations of glucose are much greater in both poultry and wild birds than in mammals which in turn are higher than in reptiles. The basis for this difference is unknown but does not appear to be related to the requirements of flight. Furthermore, birds exhibit a refractoriness to potential adverse effects of very high circulating concentrations of glucose. Again the basis of this is unclear. There is substantial information on the control of metabolism in poultry, although which hormones are exerting physiologic roles remains to be clarified. There is a tacit but unverified assumption that the control mechanisms are the same in wild birds and in poultry. Despite, significant research focus on metabolism in poultry and to a less extent wild birds, there is a dearth of studies determining metabolism in a quantitative manner.Frontiers in Biology. 04/2012; 8(2).
- [Show abstract] [Hide abstract]
ABSTRACT: The effects of glucocorticoid on lipid metabolism of broiler chicken (Gallus gallus domesticus) skeletal muscle were investigated. Male Arbor Acres chickens (35 days old) were subjected to dexamethasone treatment for 3 days. We found that dexamethasone retards body growth while facilitating lipid accumulation. In M. pectoralis major (PM), dexamethasone increased the expression of glucocorticoid receptor (GR), fatty acid transport protein 1 (FATP1), heart fatty acid-binding protein (H-FABP) and long-chain acyl-CoA dehydrogenase (LCAD) mRNA and decreased the expression of liver carnitine palmitoyltransferase 1 (L-CPT1), adenosine-monophosphate-activated protein kinase (AMPK) α2 and lipoprotein lipase (LPL) mRNA. LPL activity was also decreased. In M. biceps femoris (BF), the levels of GR, FATP1 and L-CPT1 mRNA were increased. AMPKα (Thr172) phosphorylation and CTP1 activity of skeletal muscle were decreased by dexamethasone. In fed chickens, dexamethasone enhanced very low-density lipoprotein receptor (VLDLR) expression and AMPK activity in muscle, but it impaired the expression of LPL and L-CPT1 mRNA and LPL activity in PM and augmented the expression of GR, LPL, H-FABP, L-CPT1, LCAD and AMPKα2 mRNA in BF. Adipose triglyceride lipase (ATGL) protein expression was not affected by dexamethasone. In conclusion, in the fasting state, dexamethasone-induced-retarded fatty acid utilisation may be involved in the augmented intramyocellular lipid accumulation in both glycolytic (PM) and oxidative (BF) muscle tissues. In the fed state, dexamethasone promoted the transcriptional activity of genes related to lipid uptake and oxidation in muscles. Unmatched lipid uptake and utilisation are suggested to be involved in the augmented intramyocellular lipid accumulation.Stress (Amsterdam, Netherlands) 11/2011; 15(4):443-56. · 3.46 Impact Factor