Submitted on April 24, 2007
Revised on September 18, 2007
Accepted on September 27, 2007
Conjugated linoleic acid fails to worsen insulin resistance but induces hepatic steatosis in the presence of leptin in ob/ob mice
Angela A. Wendel, Aparna Purushotham, Li-Fen Liu, and Martha A. Belury
The Ohio State University, Columbus, OH 43210
Corresponding Author: belury.1{at}osu.edu
Conjugated linoleic acid (CLA) induces insulin resistance preceded by rapid depletion of the adipokines leptin and adiponectin, increased inflammation, and hepatic steatosis in mice. To determine the role of leptin in CLA-mediated insulin resistance and hepatic steatosis, recombinant leptin was co-administered with dietary CLA in ob/ob mice to control leptin levels and to, in effect, negate the leptin depletion effect of CLA. In a 2x2 factorial design, 6-week old, male ob/ob mice were fed either a control diet or a diet supplemented with CLA and received daily, intraperitoneal injections of either leptin or vehicle for 4 weeks. In the absence of leptin, CLA significantly depleted adiponectin and induced insulin resistance, but did not increase hepatic triglyceride concentrations or adipose inflammation, marked by IL-6 and TNFa mRNA expression. Insulin resistance was, however, accompanied by increased macrophage infiltration (F4/80 mRNA) in adipose tissue. In the presence of leptin, CLA depleted adiponectin but did not induce insulin resistance or macrophage infiltration. Despite this, CLA induced hepatic steatosis. In summary, CLA worsened insulin resistance without evidence of inflammation or hepatic steatosis in mice after 4 weeks. In the presence of leptin, CLA failed to worsen insulin resistance, but induced hepatic steatosis in ob/ob mice.
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