sc-26196 and Weight-Gain

To determine whether conjugated linoleic acid (CLA)-induced body fat loss is dependent upon metabolism of CLA by Delta6-desaturase, cyclooxygenase, or lipoxygenase.. Mice were fed diets with or without CLA and inhibitors to either Delta6-desaturase (SC-26196), cyclooxygenase (aspirin), or lipoxygenase (nordihydroguaiaretic acid (NDGA)) for 2 weeks. Body fat percent, lean mass, fat pad weights, liver weight, and fatty acid concentrations were determined. A Delta6-desaturase index was calculated, and adipose tissue prostaglandin E(2) (PGE(2)) and leukotriene B(4) (LTB(4)) concentrations were determined to confirm enzyme inhibition.. Inhibition of Delta6-desaturase and cyclooxygenase were confirmed. CLA caused a loss of body fat (P < 0.001). The body fat loss was blocked (P = 0.08) by the Delta6-desaturase inhibitor at a dose that decreased (P < 0.05) the calculated index. Aspirin and NDGA had no effect on body fat and did not interact with CLA.. Inhibition of Delta6-desaturase prevented CLA from being able to cause a body fat loss. Therefore, a desaturated metabolite of CLA appears to be involved in the CLA antiobesity effect. This effect of CLA does not seem dependent upon cyclooxygenase. Because lipoxygenase activity was not blocked by NDGA, we cannot draw conclusions about its importance in mediating the antiobesity effect of CLA.

Topics: Adipose Tissue; Adiposity; Animals; Aspirin; Cyclooxygenase Inhibitors; Dietary Fats; Dinoprostone; Eating; Enzyme Inhibitors; Leukotriene B4; Linoleic Acids, Conjugated; Linoleoyl-CoA Desaturase; Lipoxygenase; Lipoxygenase Inhibitors; Liver; Male; Masoprocol; Mice; Piperazines; Prostaglandin-Endoperoxide Synthases; Time Factors; Weight Gain