Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression.
AKR/J mice fed a high fat diet were treated with a 1% (1 g/100 g) admixture of conjugated linoleic acids (CLA) for 5 wk and compared with control mice. Body weights, energy intakes and energy expenditure (EE) determined by indirect calorimetry were measured weekly. CLA treatment reduced adipose depot weights by approximately 50% but had no significant effects on either body weight or energy intake. CLA increased EE persistently by an average of 7.7% throughout the 5-wk experiment. This greater EE, despite no difference in energy intake, was sufficient to account for the lower body fat stores in the CLA-treated mice. De novo fatty acid biosynthesis in adipose tissue, measured by incorporation of deuterium-labeled water, was not decreased by CLA treatment and therefore did not explain the lower adipose lipid in these mice. Expression of uncoupling protein (UCP) in skeletal muscle, white adipose tissue and kidney was not affected by CLA treatment. In brown adipose tissue, UCP1 expression was not affected by CLA treatment. However, UCP2 expression, although quite low, was significantly greater in CLA-fed mice. We conclude that CLA acts to reduce body fat stores by chronically increasing metabolic rate. This effect on metabolic rate is likely not due to increased UCP gene expression. Furthermore, the reduced body fat is not due to decreased de novo fatty acid synthesis in white adipose tissue.
West
D B
DB
Parke-Davis Laboratory for Molecular Genetics, Alameda, CA 96501 and. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.
Blohm
F Y
FY
Truett
A A
AA
DeLany
J P
JP
D000273:Adipose Tissue / Q000033:anatomy & histology / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015152:Blotting, Northern; D002352:Carrier Proteins / Q000235:genetics*; D003903:Deuterium; D002149:Energy Intake; D004734:Energy Metabolism / Q000187:drug effects*; D005227:Fatty Acids / Q000096:biosynthesis; D015870:Gene Expression / Q000187:drug effects*; D019382:Human Growth Hormone / Q000097:blood; D007328:Insulin / Q000097:blood; D007473:Ion Channels; D019787:Linoleic Acid / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D026901:Membrane Transport Proteins; D051379:Mice; D008806:Mice, Inbred AKR; D024101:Mitochondrial Proteins; D009929:Organ Size / Q000187:drug effects; D011506:Proteins / Q000235:genetics*; D000071256:Uncoupling Protein 1; D000071246:Uncoupling Protein 2
D001786:Blood Glucose; D002352:Carrier Proteins; D005227:Fatty Acids; D007328:Insulin; D007473:Ion Channels; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D011506:Proteins; C000604371:UCP1 protein, human; C000604389:UCP2 protein, human; C000604372:Ucp1 protein, mouse; C000604390:Ucp2 protein, mouse; D000071256:Uncoupling Protein 1; D000071246:Uncoupling Protein 2; D019382:Human Growth Hormone; D019787:Linoleic Acid; D003903:Deuterium