Inhibition of acute feeding responses to systemic 2-deoxyglucose or insulin in rats pretreated with the GABA-transaminase blocker ethanolamine-O-sulfate (EOS).
Acute feeding responses to 2-deoxyglucose (750 mg/kg) or insulin (12 U/kg) were examined 24 hr after intracisternal injection of the GABA-transaminase inhibitor ethanolamine-O-sulfate (EOS, 400 micrograms) in female rats. EOS pretreatment completely abolished acute feeding responses to both challenges. These findings complement recent research showing that central EOS can reverse chronic overeating in several experimental preparations. The present results are consistent with previous indications that EOS treatment may induce a metabolic shift away from brain glucose utilization, thus making glucoprivation irrelevant as a metabolic challenge. An alternative possibility is that EOS-induced increases of brain GABA may offset specific neural mechanisms through which these glucoprivic agents normally induce feeding.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000187:drug effects; D003837:Deoxy Sugars / Q000494:pharmacology*; D003847:Deoxyglucose / Q000494:pharmacology*; D004435:Eating / Q000187:drug effects*; D004983:Ethanolamines / Q000494:pharmacology*; D005260:Female; D007276:Injections, Intraventricular; D007328:Insulin / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D000637:Transaminases / Q000037:antagonists & inhibitors*
D001786:Blood Glucose; D003837:Deoxy Sugars; D004983:Ethanolamines; D007328:Insulin; C020619:ethanolamine O-sulfate; D003847:Deoxyglucose; D000637:Transaminases; D000612:4-Aminobutyrate Transaminase