Linked Life Data

20035277

Source:http://linkedlifedata.com/resource/pubmed/id/20035277

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2010-7-28
pubmed:abstractText
It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more burning. To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat-fed mice. Maximum O(2) consumption, in vitro, was determined with a chemical uncoupler of oxidative phosphorylation (carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP)). The adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio was measured by luminescence. Mitochondria were localized by confocal microscopy with MitoTracker Green and their membrane potential (Delta psi(M)) measured using tetramethylrhodamine ethyl ester perchlorate (TMRE). The effect of N-acetylcysteine (NAC) on respiration and body composition in vivo was assessed in mice. Addition of FCCP collapsed Delta psi(M) and decreased the ATP/ADP ratio. However, we demonstrated the same rate of adipocyte O(2) consumption in the absence or presence of fuels and FCCP. Respiration was only stimulated when reactive oxygen species (ROS) were scavenged by pyruvate or NAC: other fuels or fuel combinations had little effect. Importantly, the ROS scavenging role of pyruvate was not affected by rotenone, an inhibitor of mitochondrial complex I. In addition, mice that consumed NAC exhibited increased O(2) consumption and decreased body fat in vivo. These studies suggest for the first time that adipocyte O(2) consumption may be inhibited by ROS, because pyruvate and NAC stimulated respiration. ROS inhibition of O(2) consumption may explain the difficulty to identify effective strategies to increase fat burning in adipocytes. Stimulating fuel oxidation in adipocytes by decreasing ROS may provide a novel means to shift the balance from fuel storage to fuel burning.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1930-7381
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1493-502
pubmed:dateRevised
2011-4-27
pubmed:meshHeading
pubmed-meshheading:20035277-Acetylcysteine, pubmed-meshheading:20035277-Adenosine Diphosphate, pubmed-meshheading:20035277-Adenosine Triphosphate, pubmed-meshheading:20035277-Adipocytes, pubmed-meshheading:20035277-Adipose Tissue, pubmed-meshheading:20035277-Animals, pubmed-meshheading:20035277-Carbonyl Cyanide m-Chlorophenyl Hydrazone, pubmed-meshheading:20035277-Cell Respiration, pubmed-meshheading:20035277-Dietary Fats, pubmed-meshheading:20035277-Electron Transport Complex I, pubmed-meshheading:20035277-Free Radical Scavengers, pubmed-meshheading:20035277-Male, pubmed-meshheading:20035277-Mice, pubmed-meshheading:20035277-Mice, Inbred C57BL, pubmed-meshheading:20035277-Mitochondria, pubmed-meshheading:20035277-Oxidative Phosphorylation, pubmed-meshheading:20035277-Oxidative Stress, pubmed-meshheading:20035277-Oxygen Consumption, pubmed-meshheading:20035277-Pyruvic Acid, pubmed-meshheading:20035277-Rats, pubmed-meshheading:20035277-Rats, Sprague-Dawley, pubmed-meshheading:20035277-Reactive Oxygen Species, pubmed-meshheading:20035277-Rotenone
pubmed:year
2010
pubmed:articleTitle
Respiration in adipocytes is inhibited by reactive oxygen species.
pubmed:affiliation
Obesity Research Center, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural