Another interesting finding from this study is that the rate limiting steps of fatty acid b-oxidation, Acox1, and Cpt1a are divergently expressed from weaning into adulthood. This may indicate an increased need for peroxisomal over mitochondrial b-oxidation after weaning. Acox1 mRNA Temocapril HCl expression increased steadily after birth, and this pattern has been shown at the protein level. The pattern of Cpt1a expression that was observed in this study, induced at birth then markedly decreased at weaning, parallels Cpt1a expression profiles in rats at the mRNA, protein, and activity levels. Ppara regulates the expression of Acox1 in adult mice ; however, the regulation of Cpt1a in mice is less explored. In rats, Cpt1a can be induced by administration of Clofibrate and long chain fatty acids through independent mechanisms. Regardless, because modulating fatty acid oxidation is an attractive therapeutic target for the treatment of obesity, further research into the mechanisms governing the divergent expression of Acox1 and Ctp1a in mice at the suckling-weaning transition are warranted. Elovl3 regulates the elongation of saturated and monounsaturated fatty acids. Elovl3-null mice are resistant to dietinduced obesity. We observed that, after weaning, Elovl3 mRNA expression was starkly induced; however what regulates this increase is unknown. Elovl3 expression is induced in brown fat of cold-stimulated mice by the Ppar transcription factors, and in liver of Solifenacin HCl normal mice by Srebp1 transcription factors. However, the mRNA expressions of Ppar and Srebp1 factors were not induced at weaning, suggesting that other factors may be involved in the regulation of Elovl3 expression at weaning. Further research is required to indentify these factors and may lead to novel targets for the treatment of diet-induced obesity. Stearoyl-CoA desaturases are rate limiting enzymes in the hepatic biosynthesis of monounsaturated fatty acids from saturated fatty acids. Studies using Scd1 gene deficient mice have revealed a beneficial effect of Scd1 inhibition in diet-induced obesity, hepatic steatosis, and insulin resistance.