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Differential gene expression pattern in hypothalamus of chickens during fasting-induced metabolic reprogramming: functions of glucose and lipid metabolism in the feed intake of chickens
- Source :
- Poultry science. 93(11)
- Publication Year :
- 2014
-
Abstract
- Fasting-induced hypothalamic metabolic reprogramming is involved in regulating energy homeostasis and appetite in mammals, but this phenomenon remains unclear in poultry. In this study, the expression patterns of a panel of genes related to neuropeptides, glucose, and lipid metabolism enzymes in the hypothalamus of chickens during fasting and refeeding were characterized by microarray analysis and quantitative PCR. Results showed that 48 h of fasting upregulated (P < 0.05) the mRNA expressions of orexigenic neuropeptide Y and agouti-related protein but downregulated (P < 0.05) that of anorexigenic neuropeptide pro-opiomelanocortin; growth hormone-releasing hormone; islet amyloid polypeptide; thyroid-stimulating hormone, β; and glycoprotein hormones, α polypeptide. After 48 h of fasting, the mRNA expression of fatty acid β-oxidation [peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyltransferase 1A, and forkhead box O1], energy sensor protein [sirtuin 1 (SIRT1) and forkhead box O1], and glycolysis inhibitor (pyruvate dehydrogenase kinase, isozyme 4) were enhanced, but that of fatty acid synthesis and transport associated genes (acetyl-CoA carboxylase α, fatty acid synthase, apolipoprotein A-I, endothelial lipase, and fatty acid binding protein 7) were suppressed. Liver and muscle also demonstrated similar expression patterns of genes related to glucose and lipid metabolism with hypothalamus, except for that of acetyl-CoA carboxylase α, acyl-CoA synthetase long-chain family member 4, and apolipoprotein A-I. The results of intracerebroventricular (ICV) injection experiments confirmed that α-lipoic acid (ALA, pyruvate dehydrogenase kinase, isozyme 4 inhibitor, 0.10 μmol) and NADH (SIRT1 inhibitor, 0.80 μmol) significantly suppressed the appetite of chickens, whereas 2-deoxy-d-glucose (glycolytic inhibitor, 0.12 to 1.20 μmol) and NAD(+) (SIRT1 activator, 0.08 to 0.80 μmol) increased feed intake in chickens. The orexigenic effect of NAD(+) was also blocked by cotreatment with NADH. However, ICV injection of either GW7647 (PPARα agonist) or GW6471 (PPARα antagonist) showed no effects on feed intake. Results suggested that hypothalamic glycolysis (inhibited by ALA and promoted by 2-deoxy-d-glucose) and SIRT1 (inhibited by NADH and promoted by NAD(+)), not PPARα, were probably involved in feed intake regulation in chickens.
- Subjects :
- Male
medicine.medical_specialty
Pyruvate dehydrogenase kinase
Hypothalamus
Real-Time Polymerase Chain Reaction
chemistry.chemical_compound
Random Allocation
Internal medicine
medicine
Animals
Glycolysis
Fatty acid synthesis
Injections, Intraventricular
Oligonucleotide Array Sequence Analysis
chemistry.chemical_classification
biology
Chemistry
Fatty acid
Lipid metabolism
General Medicine
Fasting
Neuropeptide Y receptor
Lipid Metabolism
Diet
Fatty acid synthase
Endocrinology
Glucose
Biochemistry
Gene Expression Regulation
biology.protein
Animal Science and Zoology
NAD+ kinase
Chickens
Subjects
Details
- ISSN :
- 00325791
- Volume :
- 93
- Issue :
- 11
- Database :
- OpenAIRE
- Journal :
- Poultry science
- Accession number :
- edsair.doi.dedup.....f9b430a785a04bb3baeef141a97a2084