Monosodium L-glutamate lesions reduce susceptibility to hypoglycemic feeding and convulsions.
Lesions of the circumventricular regions of the brain induced by neonatal administration of monosodium L-glutamate (MSG) are associated with chronic hypophagia and deficits in response to a variety of feeding challenges. These deficits occur despite the fact that, at least at high doses, MSG can produce obesity. The cause of the feeding deficits in MSG-treated animals is unknown. However, the circumventricular regions that are damaged by MSG contain high concentrations of insulin binding sites. In order to determine whether the MSG lesion alters responsiveness to circulating insulin, we have investigated the response of non-obese MSG-treated mice to doses of exogenous insulin designed either to stimulate feeding or to induce hypoglycemic convulsions. We report that MSG produces a dose-related decrease in hypoglycemic convulsions and glucoprivic feeding, suggesting that a loss in sensitivity to insulin may contribute to the MSG syndrome.
Lorden
J F
JF
Sims
J S
JS
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000187:drug effects*; D005971:Glutamates / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009474:Neurons / Q000187:drug effects; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects*; D012640:Seizures / Q000139:chemically induced*; D012970:Sodium Glutamate / Q000494:pharmacology*
D001786:Blood Glucose; D005971:Glutamates; D007328:Insulin; D012970:Sodium Glutamate