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Anorexia induced in rat by D-glucosamine deoxidized at C-1.

Abstract
The effects of D-glucosamine (2-amino-2-deoxy-D-glucose), an endogenous glucose analogue, and 1-deoxy-D-glucosamine on feeding behavior were clarified. Test solutions (24 mumol) were infused into the third cerebroventricle of the rat. Glucosamine induced a feeding episode within 30 min after infusion and then prolonged the ensuing postprandial intermeal interval for the first 4 h of the dark period, while glucose suppressed feeding by decreasing meal size. Ventricular injection of 1-deoxyglucosamine potently suppressed feeding in a dose-related manner by affecting all meal parameters, and oral administration of 2,400 mumol also induced anorexia. Changes in activity of glucose-sensitive neurons in the lateral hypothalamus and glucoreceptor neurons in the ventromedial hypothalamus after electrophoretic application of glucosamine and 1-deoxyglucosamine were compatible with behavior changes. The results indicate that replacement of a hydroxyl group by an amino group at C-2 of the glucose molecule affects feeding behavior and deoxidation of C-1 potently induces anorexia.
AuthorsK Fujimoto, T Sakata, T Shiraishi, K Kurata, K Terada, H Etou
JournalThe American journal of physiology (Am J Physiol) Vol. 251 Issue 3 Pt 2 Pg. R481-91 (Sep 1986) ISSN: 0002-9513 [Print] United States
PMID3463216 (Publication Type: Journal Article)
Chemical References
  • 1-deoxyglucosamine
  • Glucosamine
Topics
  • Administration, Oral
  • Animals
  • Anorexia (chemically induced)
  • Cerebral Ventricles (physiology)
  • Chemical Phenomena
  • Chemistry
  • Darkness
  • Drinking (drug effects)
  • Eating (drug effects)
  • Feeding and Eating Disorders (chemically induced)
  • Glucosamine (analogs & derivatives, metabolism, pharmacology)
  • Hypothalamus (cytology, drug effects, physiology)
  • Injections, Intraventricular
  • Light
  • Locomotion (drug effects)
  • Male
  • Oxidation-Reduction
  • Rats
  • Rats, Inbred Strains
  • Time Factors

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