Abstract
The impact of physiological stress on lipid metabolism, the metabolome, and systemic responses was examined in chickens. To incite a stress response, birds were continuously administered corticosterone (CORT) in their drinking water at three doses (0 mg/L, 10 mg/L, and 30 mg/L), and they were sampled 1, 5, and 12 days after commencement of CORT administration. Corticosterone administration to birds differentially regulated lipogenesis genes (i.e. FAS, ACC, ME, and SREBF1), and histopathological examination indicated lipid deposition in hepatocytes. In addition, CORT affected water-soluble metabolite profiles in the liver, as well as in kidney tissue and breast muscle; thirteen unique metabolites were distinguished in CORT-treated birds and this was consistent with the dysregulation of lipid metabolism due to physiological stress. Acute phase responses (APRs) were also altered by CORT, and in particular, expression of SAA1 was decreased and expression of CP was increased. Furthermore, CORT administration caused lymphoid depletion in the bursa of Fabricius and elevated IL6 and TGFβ2 mRNA expression after 5 and 12 days of CORT administration. Collectively, incitement of physiological stress via administration of CORT in chickens modulated host metabolism and systemic responses, which indicated that energy potentials are diverted from muscle anabolism during periods of stress.
Highlights
The impact of physiological stress on lipid metabolism, the metabolome, and systemic responses was examined in chickens
Malonyl-CoA is generated from the carboxylation of acetyl-CoA by acetyl-CoA carboxylase (ACC); this enzyme acts as the rate limiting step in fatty acid synthesis[9]
We examined the impact of administering CORT to chickens on hepatic lipid metabolism, metabolite compositions of liver, kidney and breast muscle, as well as a variety of systemic immune and stress responses
Summary
The impact of physiological stress on lipid metabolism, the metabolome, and systemic responses was examined in chickens. Corticosterone administration to birds differentially regulated lipogenesis genes (i.e. FAS, ACC, ME, and SREBF1), and histopathological examination indicated lipid deposition in hepatocytes. CORT affected water-soluble metabolite profiles in the liver, as well as in kidney tissue and breast muscle; thirteen unique metabolites were distinguished in CORT-treated birds and this was consistent with the dysregulation of lipid metabolism due to physiological stress. Incitement of physiological stress via administration of CORT in chickens modulated host metabolism and systemic responses, which indicated that energy potentials are diverted from muscle anabolism during periods of stress. Previous studies in poultry have demonstrated that physiological stress can result in increased expression of hepatic lipid synthesis genes and extrahepatic lipid deposition[4,6]. Synthesized lipids are incorporated into very-low density lipoprotein (VLDL) for secretion from the liver where they enter circulation for deposition into extrahepatic and adipose tissue[10]
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