Rapid-onset hypoglycemia is detected by glucose-sensing mechanisms within the VMH, which, in turn, stimulates autonomic output to enhance counterregulatory.

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Rapid-onset hypoglycemia is detected by glucose-sensing mechanisms within the VMH, which, in turn, stimulates autonomic output to enhance counterregulatory hormone release. Rapid-onset hypoglycemia is detected by glucose-sensing mechanisms within the VMH, which, in turn, stimulates autonomic output to enhance counterregulatory hormone release. Slow-onset hypoglycemia is detected by PMV glucose sensors, and this signal is then transmitted to hindbrain catecholaminergic centers via CSMG where they are integrated. Catecholaminergic neurons (dotted lines) then project to the PVH, where they activate neuroendocrine and autonomic centers to stimulate counterregulatory hormone responses. In addition, catecholaminergic neurons may project to VMH GABAergic terminals to provide additional input to reduce GABA release during slow-onset hypoglycemia to stimulate counterregulatory responses. Owen Chan, and Robert S. Sherwin Diabetes 2014;63:2617-2619 ©2014 by American Diabetes Association

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