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A more recent version of this article appeared on February 1, 2007

Papers In Press, published online ahead of print October 18, 2006
J. Lipid Res., doi:10.1194/jlr.M600393-JLR200
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Submitted on August 31, 2006
Revised on October 5, 2006
Accepted on October 5, 2006

Maintenance of adiponectin attenuates insulin resistance induced by dietary conjugated linoleic acid in mice

Aparna Purushotham, Angela A. Wendel, Li-Fen Liu, and Martha A. Belury

Ohio State University, Columbus, OH 43210

Corresponding Author: belury.1{at}osu.edu

Conjugated linoleic acid (CLA) causes insulin resistance and hepatic steatosis in conjunction with depletion of adipokines in some rodent models. Our objective was to determine if maintenance of adipokines mainly leptin and adiponectin by either removing CLA from diets or using an adiponectin enhancer, rosiglitazone (ROSI) could attenuate CLA induced insulin resistance. Male C57BL/6 mice were consecutively fed two experimental diets containing 1.5% CLA mixed isomer for four weeks followed by a diet without CLA for four weeks. CLA significantly depleted adiponectin, but not leptin and was accompanied by hepatic steatosis and insulin resistance. These effects were attenuated after switching mice to the diet without CLA along with restoration of adiponectin. To further elucidate the role of adiponectin in CLA mediated insulin resistance, ROSI was used in a subsequent study in male ob/ob mice fed either CON or CLA diet. ROSI maintained significantly higher adiponectin levels in CON and CLA fed mice and prevented depletion of epididymal adipose tissue and development of insulin resistance. In conclusion, we show that insulin resistance induced by CLA may be related more to adiponectin depletion than leptin and maintaining adiponectin levels alone either by removing CLA or using ROSI can attenuate these effects.


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