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1 Neurology Service, Veterans Affairs Medical Center, East Orange 07018; and 2 Department of Neurosciences and 3 Pharmacology and Physiology, New Jersey Medical School, Newark, New Jersey 07103
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
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