depletion and apoptosis induced by trans-10, cis-12 conjugated linoleic acid in mice. Obes Res. 2002;10:1284 -1290. Objective: To compare the effectiveness of a conjugated linoleic acid (CLA) isomer mixture (mCLA) with each main isomer [trans-10,cis-12 CLA (CLA10,12) and cis-9,trans-11 CLA (CLA9,11)] in causing body lipid loss and adipose tissue apoptosis. Research Methods and Procedures: Mice selected over 16 generations for high (MH) or low (ML) energy expenditure and a control group (MC) were fed diets containing either soy oil or soy oil plus mCLA, CLA10,12, or CLA9,11 for 5 days in one study and 14 days in a second study. Results: Mice fed mCLA or CLA10,12 had less body lipid (p Ͻ 0.05), smaller retroperitoneal fat pads (p Ͻ 0.05), and ate less (p Ͻ 0.01) than mice fed no CLA or CLA9,11 for 5 days. Mice consuming 1% mCLA or 0.5% CLA10,12 gained less weight (p Ͻ 0.01) and had less body lipid (p Ͻ 0.05) and smaller epididymal (p Ͻ 0.05) and retroperitoneal fat pads (p Ͻ 0.01) than mice consuming either control or 0.5% CLA9,11-containing diets for 14 days. Only mCLA and CLA10,12 increased apoptosis in retroperitoneal fat pads (p Ͻ 0.01). The effects of mCLA and CLA10,12 were independent of genetic line except for the effect on adipocyte apoptosis. Mice of the MH line were slightly less sensitive than MC or ML mice to CLA-induced adipose tissue apoptosis. Discussion: CLA10,12, but not CLA9,11, can induce both body fat loss and adipose apoptosis. Although mice of a genotype with less body fat and greater metabolic rate and feed intake appear less sensitive, these CLA effects are robust for mice of varying metabolic background.

. Influence of dietary conjugated linoleic acid and fat source on body fat and apoptosis in mice. Obes Res. 2004;12:1435-1444. Objective: To determine whether altered dietary essential fatty acid (linoleic and arachidonic acid) concentrations alter sensitivity to conjugated linoleic acid (CLA)-induced body fat loss or DNA fragmentation. Research Methods and Procedures: Mice were fed diets containing soy oil (control), coconut oil [essential fatty acid deficient (EFAD)], or fish oil (FO) for 42 days, and then diets were supplemented with a mixture of CLA isomers (0.5% of the diet) for 14 days. Body fat index, fat pad and liver weights, DNA fragmentation in adipose tissue, and fatty acid profiles of adipose tissue were determined. Results: The EFAD diet decreased (p Ͻ 0.05) linoleic and arachidonic acid in mouse adipose tissue but did not affect body fat. Dietary CLA caused a reduction (p Ͻ 0.05) in body fat. Mice fed the EFAD diet and then supplemented with CLA exhibited a greater reduction (p Ͻ 0.001) in body fat (20.21% vs. 6.94% in EFAD and EFAD ϩ CLA-fed mice, respectively) compared with mice fed soy oil. Dietary FO decreased linoleic acid and increased arachidonic acid in mouse adipose tissue. Mice fed FO or CLA were leaner (p Ͻ 0.05) than control mice. FO ϩ CLA-fed mice did not differ in body fat compared with FO-fed mice. Adipose tissue apoptosis was increased (p Ͻ 0.001) in CLA-supplemented mice and was not affected by fat source. Discussion: Reductions in linoleic acid concentration made mice more sensitive to CLA-induced body fat loss only when arachidonic acid concentrations were also reduced. Dietary essential fatty acids did not affect CLA-induced DNA fragmentation.