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Published on: March 10, 2016
Central effects of bile acids on feed intake and mRNA expression of appetite-related neuropeptides in layer-type
Elham Ghashghaei1, Ahmed Mijiyawa1, Minghui Wang1
1Key Laboratory of Efficient Utilization of Non-grain Feed Resources (Co-construction by Ministry and Province), Ministry of Agriculture and Rural Affairs, Shandong Provincial Key Laboratory of Animal Nutrition and Efficient Feeding, Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271017, China.
Abstract:
Dietary bile acids (BAs) have been shown to affect food intake in chicks; however, the underlying central mechanisms remain unclear. This study investigated the effects of taurochenodeoxycholic acid (TCDCA), sodium taurocholate (STC), chenodeoxycholic acid (CDCA), taurocholic acid (TCA), hyodeoxycholic acid (HDCA), allocholic acid (ACA), and a mixed BA (MBA; 4.6% hyodicolate, 72.6% hyodeoxycholate, and 18.3% chenodeoxycholate) on feed intake and hypothalamic mRNA expression of appetite-related neuropeptides in chicks. To determine the effects, intracerebroventricular (ICV) injections of three doses (0.25, 0.5, and 1 μg) of each BA were administered to 5-day-old layer-type chicks, and feed intake was recorded at 30, 60, and 120 minutes post-injection. Quantitative PCR was used to determine the hypothalamic mRNA expression of neuropeptide Y (NPY) and its receptors, agouti-related peptide (AgRP), pro-opiomelanocortin (POMC), and melanocortin receptors. Results showed that feed intake decreased after ICV administration of CDCA, CA, HDCA, MBA, and STC, whereas ACA and TCDCA increased intake (P < 0.05). TCDCA upregulated NPY5R, while CDCA downregulated NPY4R (P < 0.05). STC and CA increased POMC and MC4R expression and reduced AgRP (P < 0.05), whereas HDCA decreased AgRP (P < 0.05). ACA reduced MC4R expression, and MBA downregulated both NPY4R and NPY5R (P < 0.05). The result suggests that both orexigenic and anorexigenic neuropeptide genes are involved in the effects of BAs. The effect of BAs acts in a dose-dependent manner in the hypothalamus to influence feed intake.
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