No abstract

Hepatic lipogenesis-induced de novo by glucocorticoids (GCs) is associated with the development of obesity and diabetes mellitus. The interaction of GCs and insulin in the regulation of hepatic lipogenesis remains unclear. The effect of exogenous GC administration on hepatic lipogenesis and fat deposition was studied in broiler chickens (Gallus gallus domesticus), and the role of insulin in the effect of GCs on hepatic lipogenesis was evaluated. Dexamethasone (DEX, 2 mg/kg body mass (BM)) administration for 3-d resulted in BM loss and increased liver and cervical adipose tissue mass compared to control and pair-fed counterparts. DEX treatment significantly (P < 0.05) increased plasma level of insulin in either the fed or fasting state, whereas plasma glucose level was only increased in the fed state. In fasted chickens, DEX treatment significantly (P < 0.01) upregulated the hepatic mRNA levels of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). In the fed state, the mRNA levels of ACC and FAS were not significantly influenced by DEX treatment, nor was FAS activity. In cultured primary hepatocytes, combined DEX and insulin significantly upregulated the transcription of the genes for FAS (1.34-fold) and malic enzyme (1.72-fold). By contrast, the expression of sterol response element-binding protein-1 (SREBP-1) was significantly upregulated by insulin (1.67-fold) regardless of DEX. In abdominal adipose tissue, DEX treatment had no significant (P>0.05) effect on the activities and transcription of FAS. The expressions of lipoprotein lipase and peroxisome proliferator-activated receptor-γ were not significantly (P>0.05) affected by DEX treatment in either the fasting or fed state. The results indicate that DEX increased hepatic de novo lipogenesis via the increased activity and expression of lipogenic enzymes. Insulin-activated gene expression for SREBP-1 is suggested to be involved in stress-augmented hepatic lipogenesis.

Glucocorticoids (GCs) induce the activation of the central adenosine 5′-monophosphate-activated protein kinase (AMPK) signaling pathway in birds. In this study, we aimed to investigate the effects of corticosterone (CORT) supplemented in diet on the central AMPK signaling pathway in broilers. Average daily gain (ADG) was reduced by CORT treatment, and average daily feed intake (ADFI) remained unchanged. Plasma glucose (GLU), triglyceride (TG), total cholesterol (TCHO) and CORT contents were increased by CORT administration. In addition, CORT treatment decreased the relative weights of heart, spleen and bursa, and increased the relative weights of liver and abdominal fat. The glycogen contents in the liver and breast muscle were higher in the chicks treated with CORT. CORT treatment upregulated the gene expression of mammalian target of rapamycin (mTOR), glucocorticoid receptor (GR), AMP-activated protein kinase α2 (AMPKα2), neuropeptide Y (NPY), liver kinase B1 (LKB1), AMP-activated protein kinase α1 (AMPKα1), and fatty acid synthase (FAS) in the hypothalamus. Moreover, CORT treatment increased the protein levels of acetyl-coenzyme A carboxylase (ACC) phosphorylation, and total AMPK and phosphorylated AMPK in the hypothalamus. Hence, CORT administration in the diet activated the LKB1-AMPK-NPY/ACC signaling pathway in the hypothalamus of broiler.

Objective: This study aimed to investigate the effects of corticotropin-releasing factor (CRF) on the feed intake of broiler chickens and explore its influencing mechanism. Methods:The study included two trials. In trial 1, 32 male broiler chickens (Arbor Acres, Gallus gallus domesticus) were ventricle buried tubes, and they were allowed to recover for 3 days. At 8:00 AM, intracerebroventricular (ICV) injection with CRF or normal saline was performed in 10-day-old broiler chickens, which were divided into the 5, 10, and 20 µg and control (normal saline) groups according to the dose of CRF injection. In trial 2, chickens were divided into the 10 µg and control group (physiological saline) to repeat trial 1.Results: Results of trial 1 showed that the cumulative amount of feed intake in the 10 or 20 µg groups was considerably lower than that of the control group after ICV injection with CRF. The lowest amount of feed intake was obtained with the addition of 10 µg of CRF. In trial 2, the expression of ghrelin in the hypothalamus injected with 10 µg of CRF increased significantly, but the expression of ghrelin in various sections of the small intestine considerably decreased. The expression of CRF receptor subtypes 1 (CRFR1) in the hypothalamus and some parts of the small intestine remarkably increased, and the expression of CRF receptor subtypes 2 (CRFR2) increased only in the duodenum, whereas the expression of growth hormone secretagogue receptor (GHSR-1α) in the jejunum and ileum increased considerably after ICV injection of 10 µg of CRF. Conclusion:The CRF at 10 µg increased ghrelin expression in the hypothalamus and CRFR1 expression in the small intestine, and this phenomenon was related to the suppressed feed intake of broiler chickens.