hyperplasia during development that would inform the study of human obesity. It is worth noting that, despite the uncertainty about insulin signaling in chicken adipose tissue, fasting altered the expression of several messengers encoding elements of the insulin signaling cascade. Expression of PIK3CB, which encodes the catalytic p110 subunit www.selleckchem.com/products/Pazopanib-Hydrochloride.html of PI3K, was up regulated with fasting, while PIK3R1, which encodes the regulatory p85 subunit, was down regulated. Such regulation could maintain some insulin signals despite a fall in plasma insulin level. CBLB and CRK, which medi ate insulin signals that are associated with lipid rafts, were also up regulated with fasting. In mammals, this pathway stimulates glucose uptake independently of PI3K activation, which may shed light on the apparent refractoriness of PI3K activity to insulin that was described in chicken skeletal muscle.

Therefore, the potential effects of insulin on lipid storage and energy utilization appear to be defended in the fasting state, when insulin levels fall, by enhanced insulin sensitivity at the post receptor level. Additional studies are needed to confirm this effect and to further explore the poten tial of PI3K independent effects of insulin on glucose utilization in chicken adipose tissue. Insulin is not considered to be a key regulator of glu cose metabolism in chicken adipose tissue, although it does induce glucose disposal in chicken liver and muscle. It is therefore not surprising that the majority of genes significantly altered by both insulin neutralization and fasting are not related to glucose metabolism and lipid synthesis.

The main exception is DGAT2, which catalyzes the final step in esterification of fatty acids into triglycerides. In fact, DGAT2 showed the most extreme down regulation in each treatment group, which is surprising considering that other genes related Cilengitide to lipo genesis were only regulated by fasting. Suppression of DGAT2 expression may be due to feedback by lipolysis, which appeared to be increased in both treatment groups based on plasma NEFA levels. In general, our data indicate that insulin deprivation altered fatty acid and glucose metabolism in a manner comparable to fasting but to a lesser extent, such that most genes involved in these pathways did not exhibit statistically significant changes in expression.

For example, cluster analysis revealed that some genes upregulated by fasting were also increased by insulin neutralization, these three clusters were enriched with genes in the KEGG pathways for fatty acid metab olism and PPAR signaling, including both ACOX1 and CPT1A, among others. Similarly, among genes selleck chemical Lapatinib that were downregulated by fasting, clustering discriminated a set of genes with a trend to also be decreased by in sulin deprivation. Interestingly, this cluster was signifi cantly enriched in functions related to carbohydrate metabolism, suggesting that insulin does play some role in chicken adipose glucose metabolism. Comparable trends ap