Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1985-8-12
pubmed:abstractText
The objectives of this study were to evaluate the rate at which brown adipose tissue (BAT) from mice atrophies when its thermogenic activity is suppressed during fasting or exposure to a thermoneutral environment (33 degrees C) and whether such atrophy is accompanied by loss from BAT mitochondria of "thermogenin," the GDP binding protein associated with the calorigenic proton conductance pathway. Atrophy of mouse BAT was characterized by rapid loss of protein but unchanged tissue DNA content. The rate of protein loss varied from 2 to 6 mg protein/day depending on the environmental and feeding status of the mice. In synchrony with tissue protein loss, there was a marked reduction in the tissue content of mitochondrial proteins and of thermogenin, measured by immunoassay. However, the concentration of thermogenin in isolated mitochondria was unchanged by fasting or exposure of the mice to 33 degrees C for 48 h. By contrast, marked reduction in [3H]GDP binding to isolated mitochondria were observed after exposure of the mice to 33 degrees C. Mice acclimated at 4 but not those acclimated at 21 degrees C showed reduction in GDP binding to isolated mitochondria during fasting. These results clearly indicate that changes in purine nucleotide binding to isolated mitochondria can occur in the absence of changes in the mitochondrial concentration of thermogenin. Thus rapid decrease in BAT thermogenic capacity (e.g., during fasting or 33 degrees C exposure) appears dependent on extensive loss of tissue protein, probably whole mitochondria, rather than rapid and selective removal of thermogenin from the mitochondria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
249
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E99-106
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:3925790-Acclimatization, pubmed-meshheading:3925790-Adipose Tissue, Brown, pubmed-meshheading:3925790-Animals, pubmed-meshheading:3925790-Atrophy, pubmed-meshheading:3925790-Body Temperature, pubmed-meshheading:3925790-Body Weight, pubmed-meshheading:3925790-Carrier Proteins, pubmed-meshheading:3925790-DNA, pubmed-meshheading:3925790-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:3925790-Fasting, pubmed-meshheading:3925790-Guanosine Diphosphate, pubmed-meshheading:3925790-Immunodiffusion, pubmed-meshheading:3925790-Ion Channels, pubmed-meshheading:3925790-Male, pubmed-meshheading:3925790-Membrane Proteins, pubmed-meshheading:3925790-Mice, pubmed-meshheading:3925790-Mitochondria, pubmed-meshheading:3925790-Mitochondrial Proteins, pubmed-meshheading:3925790-Oxygen Consumption, pubmed-meshheading:3925790-Proteins, pubmed-meshheading:3925790-Temperature
pubmed:year
1985
pubmed:articleTitle
Mitochondrial thermogenin content is unchanged during atrophy of BAT of fasting mice.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't