Obesity is associated with insulin resistance, which is a central component of non-insulin-dependent diabetes mellitus (NIDDM) (1). Several substances have been implicated in the etiology of insulin resistance, such as circulating free fatty acids (FFAs), as well as tumor necrosis factor-α (TNF-α) and leptin produced by the adipocytes.
In a recent report from Bruce M Spiegelman's laboratory by Hotamisligil et al. (2) a possible functional role for FFAs in adipocytes was studied by creating a mouse strain lacking the adipocyte fatty acid-binding protein (aFABP). A null mutation was introduced in the aP2 gene encoding the aFABP, and the mice were crossed to create offspring homozygous for the null mutation (aP2 −/− mice). The resulting inbred homozygous aP2 mutant mice lacked aFABP in their adipocytes, but did not differ phenotypically from their wild-type (aP2 +/+) or heterozygous (aP2 +/−) littermates under standard feeding conditions. The lack of obvious differences in metabolic phenotype