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Recurrent hypoglycemia impairs these protective mechanisms, resulting in a potentially life\u2010threatening condition known as hypoglycemia\u2010associated autonomic failure (HAAF). During HAAF, the glycemic threshold is reset so that glucose levels must fall further before the CRR is initiated. The brain plays a critical role in sensing hypoglycemia and initiating the CRR. Additionally, many neurons may sense changes in plasma and extracellular glucose. However, the way in which central glucose sensing is integrated to lead to effective initiation of the CRR is unknown. Furthermore, the mechanisms by which this system becomes impaired during HAAF are also unknown. Glucosensing neurons in the ventromedial hypothalamic nucleus (VMN) are poised to serve an integrative function in glucose homeostasis. First, they sense glucose. Second, the VMN receives input from other glucose\u2010sensing areas. Finally, the VMN projects to areas linked to the regulation of the sympathoadrenal system that mediates the CRR. This review discusses VMN glucosensing neurons relative to their capacity to play a role in the regulation of the CRR and the generation of HAAF. Glucosensing neurons in the hindbrain as well as peripheral glucosensors are also considered. 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