Growing evidence suggests that insulin interacts with both orexigenic and anorexigenic peptides in the brain for the control of feeding behavior in mammals. However, the action of central insulin in chicks has not yet been identified. In the present study, we investigated the effects of central injection of insulin on feeding behavior in chicks. Intracerebroventricular (ICV) administration of insulin, at doses that do not influence peripheral glucose levels, significantly inhibited food intake in chicks. Central injection of insulin in chicks significantly increased expression of pro-opiomelanocortin (POMC) mRNA, and decreased that of neuropeptide Y (NPY) mRNA. Finally, co-injection of the melanocortin antagonist (SHU9119 or HS014) prevented the reduction in food intake caused by ICV administration of insulin. These data suggest that insulin functions in chicks as an appetite-suppressive peptide in the central nervous system, and that the central melanocortin system mediates this anorexic effect of insulin, as in mammals.

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Regulation of feed intake in chickens represents a complex homeostatic mechanism involving multiple levels of control. Understanding the regulation of feeding behavior can be a very important theme in animal production. Recently, a close evolutionary relationship between the peripheral and hypothalamic neuropeptides has become apparent. In the infundibular nucleus (the avian equivalent of the mammalian arcuate nucleus), the melanocortin system, which contains neuroendocrine neurons that regulate endocrine secretions by releasing substances, is an essential site in the brain for signals about the status of peripheral energy balance. The structure and function of many hypothalamic neuropeptides, melanocortins, neuropeptide-Y (NPY) and agouti-related protein (AGRP) have been characterized. This review provides as overview of the various e ects and interrelationship of these central and peripheral neuropeptides, and summarizes the role of the melanocortin system on feeding regulation in chicks.

It is known that thermal conditioning at an early age results in improved heat tolerance, and reduces mortality when re-exposed to heat in later life in chickens. However, the mechanism of thermal conditioning is not fully understood. The objective of this study was to investigate the effect of early thermal conditioning on physiological and behavioral responses in acute heat-exposed chicks. Six-day-old chicks (White Plymouth Rock) were exposed to high temperature at 40℃ for 3 h while control chicks were kept at 30℃. Four days after treatment, both groups were challenged to high temperature at 40℃ for 15 min. We found that the initiation times for behavioral responses (panting and wing-droop posture) in experienced chicks were later than those in control. At the end of heat-exposure treatment, the rectal temperature in experienced chicks was lower than that in control while there was no difference in respiration rate between the groups. Compared with control, experienced chicks had a lower level of plasma corticosterone. Gene expression levels of brain-derived neurotrophic factor, thyrotropin-releasing hormone, interleukin-6 and lipopolysaccharide-induced tumor necrosis factor were significantly lower in the brain of experienced chicks than in the control chicks. These results suggest that thermal conditioning may change response to subsequent heat exposure by altering the central thermoregulation system, resulting in an alleviation of heat stress.