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Diabetes Publish Ahead of Print published online ahead of print January 24, 2007
DOI: 10.2337/db06-1206
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Original Research

N-3 Fatty Acids Preserve Insulin Sensitivity In Vivo in a PPAR{alpha}-Dependent Manner

Susanne Neschen1,,2, Katsutaro Morino1,,2, Jianying Dong1, Yanlin Wang-Fischer1, Gary W. Cline1, Anthony J. Romanelli1, Jörg C. Rossbacher3, Irene K. Moore2, Werner Regittnig2, David S. Munoz2, Jung H. Kim4, and Gerald I. Shulman1,,2,,4

1Howard Hughes Medical Institute and the Departments of
2Internal Medicine, Cellular & Molecular Physiology
3Laboratory Medicine
4Pathology, Yale University School of Medicine, New Haven, CT

Correspondence: gerald.shulman{at}yale.edu

Recent studies have suggested that n-3 fatty acids, abundant in fish oil, protect against high-fat diet-induced insulin resistance through PPAR{alpha} activation and a subsequent decrease in intracellular lipid abundance. To directly test this hypothesis we fed PPAR{alpha} null and wild type (WT) mice for two weeks with isocaloric high-fat diets containing 27% fat from safflower oil (SAFF) or safflower oil with an 8% fish oil replacement (FISH). In both genotypes SAFF diet blunted the insulin-mediated suppression of hepatic glucose production (P<0.02 vs. genotype CONT) and PEPCK gene expression. In WT mice FISH feeding restored hepatic insulin sensitivity (HGP, P<0.002 vs. WT SAFF) whereas in contrast, in PPAR{alpha} null mice FISH feeding failed to counteract hepatic insulin resistance (HGP n.s. vs. PPAR{alpha} null SAFF). Hepatic insulin resistance in FISH fed PPAR{alpha} null mice was dissociated from increases in hepatic triacylglycerol and acyl-CoA but accompanied by a more than three-fold increase in hepatic diacylglycerol concentrations (P<0.0001 vs. genotype CONT). These data support the hypothesis that n-3 fatty acids protect from high-fat diet-induced hepatic insulin resistance in a PPAR{alpha} and diacylglycerol dependent manner.


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