Abstract
The brain has evolved mechanisms for sensing and regulating glucose metabolism. It receives neural inputs from glucosensors in the periphery but also contains neurons that directly sense changes in glucose levels by using glucose as a signal to alter their firing rate. Glucose-responsive (GR) neurons increase and glucose-sensitive (GS) decrease their firing rate when brain glucose levels rise. GR neurons use an ATP-sensitive K+ channel to regulate their firing. The mechanism regulating GS firing is less certain. Both GR and GS neurons respond to, and participate in, the changes in food intake, sympathoadrenal activity, and energy expenditure produced by extremes of hyper- and hypoglycemia. It is less certain that they respond to the small swings in plasma glucose required for the more physiological regulation of energy homeostasis. Both obesity and diabetes are associated with several alterations in brain glucose sensing. In rats with diet-induced obesity and hyperinsulinemia, GR neurons are hyporesponsive to glucose. Insulin-dependent diabetic rats also have abnormalities of GR neurons and neurotransmitter systems potentially involved in glucose sensing. Thus the challenge for the future is to define the role of brain glucose sensing in the physiological regulation of energy balance and in the pathophysiology of obesity and diabetes.
- insulin
- food intake
- sulfonylureas
- ATP-sensitive K+ channel
- neuropeptide Y
- diet-induced obesity
- autonomic nervous system
- sympathetic nervous system
- parasympathetic nervous system
- ventromedial hypothalamus
- paraventricular hypothalamus
- arcuate nucleus
- hypoglycemia
Footnotes
Address for reprint requests and other correspondence: B. E. Levin, Neurology Service (127C), VA Medical Center, E. Orange, NJ 07018-1095 (E-mail: levin{at}umdnj.edu).
- Copyright © 1999 the American Physiological Society












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