Increased feeding after treatment with fructose, but not glucose, antimetabolites in rats with dopamine-depleting brain lesions

doi:10.1016/0006-8993(93)90621-S

Brain Research

Volume 617, Issue 1, 16 July 1993, Pages 120-122

https://doi.org/10.1016/0006-8993(93)90621-S Get rights and content

Abstract

Rats were given dopamine-depleting lesions either as adults or as neonates. Compared with intact controls, lesioned rats failed to increase their food intake after acute administration of the glucoprivic agent, 2-deoxy-d-glucose. In contrast, both lesioned and control rats increased food intake after acute treatment with a peripherally-acting fructose antimetabolite, 2,5-anhydro-d-mannitol. These data suggest that the failure of lesioned rats to respond behaviorally to glucoprivation is related to inhibition of glycolysis in the brain, rather than the acute nature of the metabolic challenge.

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Citation Excerpt :
Despite observations that the DD mice mount appropriate physiological changes in response to 2-DG, the behavioral response appears to depend on dopamine. Our results are similar to those obtained in lateral hypothalamic and 6-OHDA lesion models [6,15,37], and suggest that dopamine is needed to facilitate feeding in response to glucoprivation. However, because DD mice and 6-OHDA-treated rats are deficient in many goal-directed behaviors, the lack of effect of glucoprivation on feeding may be nonspecific.
Dopamine-deficient (DD) mice become hypophagic and die of starvation by 3 to 4 weeks of age unless dopamine is restored by daily treatment with l-3-4-dihydroxyphenylalanine (l-dopa). We demonstrate here that DD mice mount qualitatively normal counter-regulatory blood glucose responses to insulin and 2-deoxy-d-glucose (2-DG). However, unlike control mice, DD mice fail to eat in response to acute glucoprivation induced by insulin or 2-DG. They also have a severely blunted response to central administration of peptide YY (PYY). Viral-mediated restoration of dopamine synthesis to the central caudate putamen (CPu) of DD mice rescues feeding and survival. However, this treatment fails to restore insulin- and 2-DG-induced feeding despite normalizing feeding in response to food deprivation and PYY. Since dopamine signaling in the CPu is not sufficient for glucoprivation-induced feeding, we propose that this feeding behavior may be mediated by dopamine in an anatomically distinct brain region.
Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons
2014, American Journal of Physiology - Regulatory Integrative and Comparative Physiology

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Increased feeding after treatment with fructose, but not glucose, antimetabolites in rats with dopamine-depleting brain lesions

Abstract

Brain Res.

Neurosci. Lett.

Neurosci. Lett.

Neurosci. Lett.

Brain Res.

Brain Res. Bull.

Physiol. Behav.