Decreased nutritional responsiveness of S6K1 in the breast muscle of genetically fat chickens

摘要

S6K1 is a major effector of cell growth. For example, mice deficient for this kinase are smaller than controls and have reduced muscle mass (Ohanna et al, 2005). In mammals, S6K1 is phosphorylated in response to insulin via a signal transduction pathway involving phosphatidylinositol 3'kinase (PI3K), protein kinase B (PKB also called AKT) and the mammalian target of rapamycin (mTOR). Surprisingly, S6K1 is activated by refeeding and insulin in chicken muscle despite a relative insulin resistance in the early steps of insulin receptor signalling in this tissue (PI3K pathway) (Tesseraud et al., 2006; Duchene et al., 2007a). The Mitogen-activated protein kinase (MAPK) / Extracellular signal-regulated protein kinase (ERK) 1/2 pathway may participate in the insulin-dependent regulation of S6K1 in chicken muscle as shown in avian cells (Duchene et al., 2007b).