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type:text, 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.

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.

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.

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.