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Regulatory, Integrative and Comparative Physiology

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Brain glucose sensing and body energy homeostasis: role in obesity and diabetes

Barry E. Levin, Ambrose A. Dunn-Meynell, Vanessa H. Routh
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 May 1999 Vol. 276 no. 5, R1223-R1231 DOI:
Barry E. Levin
Neurology Service, Veterans Affairs Medical Center, East Orange 07018; and Department of Neurosciences and
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Ambrose A. Dunn-Meynell
Neurology Service, Veterans Affairs Medical Center, East Orange 07018; and Department of Neurosciences and
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Vanessa H. Routh
Department of Neurosciences and Pharmacology and Physiology, New Jersey Medical School, Newark, New Jersey 07103
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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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Keywords

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
  • Article
    • Abstract
    • ANATOMY AND PHYSIOLOGY OF GLUCOSE-SENSING NEURONS
    • ROLE OF GLUCOSE-SENSING NEURONS IN ENERGY BALANCE
    • BRAIN GLUCOSE SENSING IN OBESITY AND DIABETES
    • SUMMARY AND CONCLUSIONS
    • Footnotes
    • REFERENCES
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Brain glucose sensing and body energy homeostasis: role in obesity and diabetes
Barry E. Levin, Ambrose A. Dunn-Meynell, Vanessa H. Routh
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology May 1999, 276 (5) R1223-R1231;

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Brain glucose sensing and body energy homeostasis: role in obesity and diabetes
Barry E. Levin, Ambrose A. Dunn-Meynell, Vanessa H. Routh
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology May 1999, 276 (5) R1223-R1231;
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