Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-7-20
pubmed:abstractText
Activation of C5L2, a G-protein-coupled receptor, by acylation-stimulating protein/complement C3adesArg (ASP/C3adesArg) has been shown to stimulate triglyceride (TG) synthesis in both mature adipocytes and preadipocytes. ASP is an adipocyte-derived hormone that acts by increasing diacylglycerol acyltransferase activity and glucose transport. ASP-deficient mice (C3KO, precursor protein) are lean, display delayed postprandial TG clearance, increased food intake, and increased energy expenditure. The present study shows that C5L2KO mice on a low fat diet are hyperphagic (~60% increase in total food intake) yet maintain the same body weight and adipose tissue mass as wild-type (WT) controls. However, on a high fat diet, average adipocyte size and adipose tissue TG/DNA content were significantly reduced and postprandial TG clearance was delayed in C5L2KO. Adipose tissue TG synthesis (WT: 47.2 +/- 5.6 versus C5L2KO: 7.8 +/- 1.8 pmol/microg protein, P < 0.001), TG lipolysis (WT: 227.6 +/- 36.4 versus C5L2KO: 45.8 +/- 5.0 nmol/microg protein, P < 0.001), and fatty acid re-esterification (WT: 85.3 +/- 2.4% versus C5L2KO: 59.5 +/- 6.8%, P < 0.001) were significantly reduced in C5L2KO mice. Indirect calorimetry measurements revealed C5L2KO mice have unchanged oxygen consumption levels yet reduced respiratory quotient value, suggesting preferential fatty acid utilization over carbohydrate. In agreement, fatty acid oxidation was elevated in heart and skeletal muscle tissue in C5L2KO mice and skeletal muscle levels of uncoupling protein 3 (425.5 +/- 86.3%, P < 0.0001), CD36 (277.6 +/- 49.5%, P < 0.05), cytochrome c (252.6 +/- 33.9%, P < 0.05), and phospho-acetyl CoA carboxylase (118.4 +/- 9.3%, P < 0.05) were significantly increased in C5L2KO mice versus WT (100%). The study shows that in response to reduced TG storage in white adipose tissue, C5L2KO mice have developed a compensatory mechanism of increased muscle fat oxidation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
194
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
293-304
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17641279-Adipose Tissue, pubmed-meshheading:17641279-Animals, pubmed-meshheading:17641279-Biological Markers, pubmed-meshheading:17641279-Calorimetry, Indirect, pubmed-meshheading:17641279-Cytochromes c, pubmed-meshheading:17641279-Diet, pubmed-meshheading:17641279-Enzyme Activation, pubmed-meshheading:17641279-Fatty Acids, pubmed-meshheading:17641279-Female, pubmed-meshheading:17641279-Ion Channels, pubmed-meshheading:17641279-Lipogenesis, pubmed-meshheading:17641279-Male, pubmed-meshheading:17641279-Mice, pubmed-meshheading:17641279-Mice, Knockout, pubmed-meshheading:17641279-Mitochondrial Proteins, pubmed-meshheading:17641279-Muscle, Skeletal, pubmed-meshheading:17641279-Myocardium, pubmed-meshheading:17641279-Obesity, pubmed-meshheading:17641279-Oxygen Consumption, pubmed-meshheading:17641279-Postprandial Period, pubmed-meshheading:17641279-Protein Kinases, pubmed-meshheading:17641279-Receptors, Chemokine, pubmed-meshheading:17641279-Triglycerides
pubmed:year
2007
pubmed:articleTitle
Reduced adipose tissue triglyceride synthesis and increased muscle fatty acid oxidation in C5L2 knockout mice.
pubmed:affiliation
Department of Biochemistry, McGill University, Montreal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't