Adipocyte membrane glycerol permeability is involved in the anti-adipogenic effect of conjugated linoleic acid.

Conjugated linoleic acid (CLA), a group of minor fatty acids from ruminant origin, has long been recognized as a body fat lowering agent. Given the trans(t)10,cis(c)12-CLA well documented interference on lipolysis, we hypothesized for adipocytes altered permeation to glycerol when supplemented with this isomer. 3T3-L1 murine differentiated adipocytes were medium supplemented with linoleic acid (LA) and individual or combined c9,t11 and t10,c12-CLA isomers. Adipocytes treated with the t10,c12-CLA isomer and CLA mixture showed reduced triacylglycerols content (p < 0.001), re-enforcing the t10,c12-CLA as the anti-adipogenic CLA isomer. This finding was supported by decreased Δ9-desaturase index and adipocyte differentiation markers for the t10,c12-CLA group (p < 0.001), which suggest reduced lipogenesis and differentiation, respectively. The glycerol permeability was higher in all CLA treated cells compared to control and LA groups (p < 0.05). The increase in glycerol permeability agrees with both reduced triacylglycerols and non-osmotic cellular volume in the t10,c12-CLA and CLA mixture groups. Taken together, our data suggest that the increased adipocyte plasma membrane glycerol fluxes may be part of the anti-adipogenic response to CLA treatments.

Conjugated linoleic acid reduces permeability and fluidity of adipose plasma membranes from obese Zucker rats.

Conjugated linoleic acid (CLA) is a dietary fatty acid frequently used as a body fat reducing agent whose effects upon cell membranes and cellular function remain unknown. Obese Zucker rats were fed atherogenic diets containing saturated fats of vegetable or animal origin with or without 1% CLA, as a mixture of cis(c)9,trans(t)11 and t10,c12 isomers. Plasma membrane vesicles obtained from visceral adipose tissue were used to assess the effectiveness of dietary fat and CLA membrane incorporation and its outcome on fluidity and permeability to water and glycerol. A significant decrease in adipose membrane fluidity was correlated with the changes observed in permeability, which seem to be caused by the incorporation of the t10,c12 CLA isomer into membrane phospholipids. These results indicate that CLA supplementation in obese Zucker rats fed saturated and cholesterol rich diets reduces the fluidity and permeability of adipose membranes, therefore not supporting CLA as a body fat reducing agent through membrane fluidification in obese fat consumers.