Insulin is reciprocally regulated with the stress hormone corticosterone, consistent with the idea that it provides inhibitory tone to the
hypothalamus-adrenal-pituitary axis. Disruptions of insulin receptor (InsR) signals in Nkx2.1
-expressing regions of the hypothalamus result in elevated arginine vasopressin (AVP) levels at baseline and heightened neuroendocrine responses to restraint stress. In contrast, disrupting InsR signals in neurons of the arcuate nucleus of the hypothalamus expressing
leads to reduced AVP release in the median eminence.
This issue's cover illustrates the complicated crosstalk between energy status and stress reactivity mediated by the insulin receptor.Full Text