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Related Experiment Videos

Feeding modulation by pentose and hexose analogues.

T Sakata1, M Kurokawa

  • 1Department of Internal Medicine I, Medical College of Oita, Japan.

The American Journal of Clinical Nutrition
|January 1, 1992
PubMed
Summary

D-Glucosamine (GlcN) and 2,5-anhydro-D-mannitol (2,5-AM) stimulate feeding by altering brain activity and metabolism. N-acetyl-D-glucosamine (GlcNAc) also induces feeding, but requires oral administration and vagal nerve signaling.

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Area of Science:

  • Neuroscience
  • Metabolism
  • Endocrinology

Background:

  • The central nervous system plays a critical role in regulating food intake and energy balance.
  • Understanding the molecular mechanisms underlying appetite control is crucial for addressing metabolic disorders.
  • Specific carbohydrate derivatives may act as signaling molecules influencing feeding behavior.

Purpose of the Study:

  • To investigate the effects of D-glucosamine (GlcN), N-acetyl-D-glucosamine (GlcNAc), and 2,5-anhydro-D-mannitol (2,5-AM) on food intake in rats.
  • To explore the neurobiological and metabolic pathways modulated by these compounds.
  • To elucidate their potential as probes for studying central feeding regulation.

Main Methods:

  • Intracerebroventricular (icv) infusion of GlcN, GlcNAc, and 2,5-AM in rats.
  • Oral administration of GlcNAc.
  • Measurement of plasma glucose, free fatty acids, glycerol, and insulin levels.
  • Electrophysiological recording of neuronal activity in the lateral hypothalamic area (LHA) and ventromedial hypothalamus (VMH).
  • Bilateral truncal vagotomy to assess the role of the vagus nerve.

Main Results:

  • GlcN (24 mumols/L icv) accelerated eating and increased plasma glucose, free fatty acids, and glycerol, while decreasing VMH and increasing LHA neuronal activity.
  • GlcNAc (12 mumols/L icv) did not affect feeding, but oral administration (1200 mumols/L) induced feeding, which was abolished by vagotomy.
  • 2,5-AM dose-dependently induced feeding (P < 0.01) upon icv infusion, with a maximal dose (24 mumols/L) not significantly altering plasma glucose or insulin.
  • Microinfusion of 2,5-AM into the VMH, but not the LHA, elicited feeding.

Conclusions:

  • GlcN and 2,5-AM directly influence central feeding control mechanisms.
  • GlcNAc-induced feeding is mediated by the vagus nerve, suggesting peripheral signaling pathways.
  • These carbohydrate analogues serve as valuable tools for dissecting the complex interplay between energy metabolism and central appetite regulation.

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