Reduction in voluntary food intake, but not fasting, stimulates hypothalamic gonadotropin-inhibitory hormone precursor mRNA expression in chicks under heat stress.

Heat stress is an issue of rising concern across the globe. Recently, we found that mRNA expression of gonadotropin-inhibitory hormone (GnIH), an orexigenic neuropeptide, was increased in the heat-exposed chick brain when food intake was reduced. The aim of the current study was to examine mRNA expression of GnIH and of the glucocorticoid receptors (GRs) in the hypothalamus as well as the plasma corticosterone (CORT) and metabolites in 14-d-old chicks exposed to a high ambient temperature (HT; 40 ±â€¯1 °C for 1 or 5 h) or a control thermoneutral temperature (CT; 30 ±â€¯1 °C), either with free access to food or fasted. Heat stress caused a voluntary reduction of food intake and reduced plasma triacylglycerol concentration, but increased rectal temperature and plasma CORT and glucose concentrations (P < 0.05). Heat stress also increased (P < 0.05) the expression of diencephalic GnIH mRNA in chicks when they reduced food intake voluntarily, but did not do so under fasting conditions. Although the expression of GR mRNA was not altered as a result of heat stress, its expression was decreased (P < 0.05) in fasted chicks at 5 h in comparison with fed chicks. In addition, the rectal temperature of fasted chicks was lower than that of fed chicks under both CT and HT. In conclusion, voluntary reduction of food intake caused an increase in brain GnIH mRNA expression, plasma CORT, and body temperature in chicks under heat stress. Interestingly, brain GnIH mRNA expression was not induced by heat stress in fasted chicks and was not accompanied by a decrease in rectal temperature. These results suggest that the increased expression of brain GnIH mRNA in chicks under heat stress could be a consequence of a mechanism mediated by the voluntary reduction of food intake, but that it is not a consequence of fasting.

L-Citrulline acts as potential hypothermic agent to afford thermotolerance in chicks.

Recently we demonstrated that L-citrulline (L-Cit) causes hypothermia in chicks. However, the question of how L-Cit mediates hypothermia remained elusive. Thus, the objective of this study was to examine some possible factors in the process of L-Cit-mediated hypothermia and to confirm whether L-Cit can also afford thermotolerance in young chicks. Chicks were subjected to oral administration of L-Cit along with intraperitoneal injection of a nitric oxide synthase (NOS) inhibitor, NG-nitro-l-arginine methyl ester HCl (L-NAME), to examine the involvement of NO in the process of hypothermia. Food intake and plasma metabolites were also analyzed after oral administration of L-Cit in chicks. To examine thermotolerance, chicks were orally administered with a single dose of L-Cit (15mmol/10ml/kg body weight) or the same dose twice within a short interval of 1h (dual oral administration) before the exposure to high ambient temperature (35 ± 1°C) for 180min. Although the rectal temperature was reduced following administration of L-Cit, L-NAME caused a greater reduction. L-NAME reduced total NO2 and NO3 (NOx) in plasma, which confirmed its inhibitory effect on NO. A single oral administration of L-Cit mediated a persistent state of hypothermia for the 300min of the study without affecting food intake. It was further found that plasma glucose was significantly lower in L-Cit-treated chicks. Dual oral administration of L-Cit, but not a single oral administration, afforded thermotolerance without a significant change in plasma NOx in chicks. In conclusion, our results suggest that L-Cit-mediated hypothermia and thermotolerance may not be involved in NO production. L-Cit-mediated thermotolerance further suggests that L-Cit may serve as an important nutritional supplement that could help in coping with summer heat.

Chronic oral administration of pine bark extract (flavangenol) attenuates brain and liver mRNA expressions of HSPs in heat-exposed chicks.

Exposure to a high ambient temperature (HT) can cause heat stress, which has a huge negative impact on physiological functions. Cellular heat-shock response is activated upon exposure to HT for cellular maintenance and adaptation. In addition, antioxidants are used to support physiological functions under HT in a variety of organisms. Flavangenol, an extract of pine bark, is one of the most potent antioxidants with its complex mixture of polyphenols. In the current study, chronic (a single daily oral administration for 14 days) or acute (a single oral administration) oral administration of flavangenol was performed on chicks. Then the chicks were exposed to an acute HT (40±1°C for 3h) to examine the effect of flavangenol on the mRNA expression of heat-shock protein (HSP) in the brain and liver. Rectal temperature, plasma aspartate aminotransferase (AAT), a marker of liver damage, and plasma corticosterone as well as metabolites were also determined. HSP-70 and -90 mRNA expression, rectal temperature, plasma AAT and corticosterone were increased by HT. Interestingly, the chronic, but not the acute, administration of flavangenol caused a declining in the diencephalic mRNA expression of HSP-70 and -90 and plasma AAT in HT-exposed chicks. Moreover, the hepatic mRNA expression of HSP-90 was also significantly decreased by chronic oral administration of flavangenol in HT chicks. These results indicate that chronic, but not acute, oral administration of flavangenol attenuates HSP mRNA expression in the central and peripheral tissues due to its possible role in improving cellular protective functions during heat stress. The flavangenol-dependent decline in plasma AAT further suggests that liver damage induced by heat stress was minimized by flavangenol.