Linked Life Data

3237826

Source:http://linkedlifedata.com/resource/pubmed/id/3237826

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-5-4
pubmed:abstractText
We examined the interaction of the metabolic fuels, glucose and free fatty acids (FFA), in the control of food intake in Syrian hamsters. Hamsters were treated with a 2-deoxy-D-glucose (2DG) which inhibits glucose utilization, and methyl palmoxirate (MP), which inhibits fatty acid oxidation. The 2DG and MP, alone or in combination did not enhance food intake in hamsters fed a standard rodent chow diet. Determination of the circulating glucose, FFAs, and ketones confirmed that the drugs were having the intended metabolic effects. The 2DG caused marked hyperglycemia and decreased ketones consistent with an inhibition of glycolysis, and the MP caused increased FFAs and decreased ketones indicating inhibition of fatty acid oxidation. A third experiment examined the hamsters' willingness to ingest a diet made highly unpalatable with NaCl, another measure of hunger motivation. Although food-deprived hamsters ingested more of a salt-adulterated diet than did control animals, hamsters treated with MP and 2DG did not. These experiments provide further evidence that the control of food intake in Syrian hamsters is appreciably different than that of laboratory rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0031-9384
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Inhibition of fatty acid oxidation and glucose metabolism does not affect food intake or hunger motivation in Syrian hamsters.
pubmed:affiliation
Neuroscience and Behavior Program, University of Massachusetts, Amherst 01003.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.