The muscle fatty acid profile was, however, unaltered in the LBW CD offspring muscle, prompting further investigation into mitochondrial and amino acid metabolism readouts as an alternative theory to explain the observed increased PKCε in the muscle of LBW offspring because overexpression of PKCε is causally related to the development of insulin resistance, possibly by increasing the degradation of insulin receptors [79]. This evidence concerns the gene PRKCE and Insulin resistance.