RGD Reference Report - Anorectic potency of inhibiting GABA transaminase in brain: studies of hypothalamic, dietary and genetic obesities. - Rat Genome Database

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Anorectic potency of inhibiting GABA transaminase in brain: studies of hypothalamic, dietary and genetic obesities.

Authors: Coscina, DV  Nobrega, JN 
Citation: Coscina DV and Nobrega JN, Int J Obes. 1984;8 Suppl 1:191-200.
RGD ID: 10047083
Pubmed: PMID:6534893   (View Abstract at PubMed)

A variety of recent literature suggests that brain gamma-aminobutyric acid (GABA) plays an important role in the control of feeding. One such line of evidence is that pharmacological inhibition of brain GABA transaminase (GABA-T) produces dose-dependent anorexia in otherwise normal rats. To determine the generality of these findings we tested the ability of the GABA-T inhibitor ethanolamine-O-sulfate (EOS), to produce anorexia in three animal models of obesity: rats with medial hypothalamic lesions, rats exposed to palatable foods or Zucker fatty rats. Following intracisternal injection of 100, 200 or 400 micrograms EOS, all three models of chronic overeating showed dose-dependent anorexia of similar magnitude and duration to that seen in appropriate controls. These observations provide empirical support for previous suggestions that treatments which enhance brain GABA neurotransmission merit investigation for their potential use in treating excess energy consumption.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Anorexia  ISOAbat (Rattus norvegicus)10047083; 10047083 RGD 
Anorexia  IMP 10047083 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Abat  (4-aminobutyrate aminotransferase)

Genes (Mus musculus)
Abat  (4-aminobutyrate aminotransferase)

Genes (Homo sapiens)
ABAT  (4-aminobutyrate aminotransferase)


Additional Information