Conjugated Linoleic Acid (CLA) Regulates PPAR-Responsive Genes and Improves
Characteristics of the Metabolic Syndrome in Insulin-Resistant Obese Rats
A potential mechanism for CLA action is activation of peroxisomal proliferator-activated receptors (PPARs), ligand-activated transcription factors involved in lipid and glucose metabolism. Our objective was to investigate whether dietary CLA alters body fat, glucose tolerance, adipokine synthesis and PPAR-responsive gene expression in insulin-resistant obese rats. Weanling lean and fa/fa male Zucker rats were fed a 1.5% CLA mixture (lnCLA and faCLA groups) or control diet (lnCTL and faCTL groups) for 8 wks. Final body and fat pad weights were not different between CLA and CTL groups. Oral glucose tolerance was significantly improved in the faCLA rats, concomitant with reduced pancreatic B-cell hypertrophy and less fatty liver. Measurement of adipokine expression showed that leptin and TNF-alpha mRNA was reduced (~1.5 fold and 2-3 fold, respectively), while resistin was up-regulated (2-fold) in adipose tissue from faCLA rats. The mRNA levels of the PPAR-responsive fatty acid binding protein (L-FABP) and acyl-CoA oxidase genes were elevated in liver of faCLA rats. Our results indicate that a dietary CLA mixture improves oral glucose tolerance, reduces fatty liver and attenuates B-cell hypertrophy in fa/fa Zucker rats, and that activation of PPAR-responsive genes may be involved in altering metabolism.