[HTML][HTML] Insulin-induced activation of atypical protein kinase C, but not protein kinase B, is maintained in diabetic (ob/ob and Goto-Kakazaki) liver: contrasting insulin …
ML Standaert, MP Sajan, A Miura, Y Kanoh… - Journal of Biological …, 2004 - ASBMB
Insulin resistance in type 2 diabetes is characterized by defects in muscle glucose uptake
and hepatic overproduction of both glucose and lipids. These hepatic defects are perplexing
because insulin normally suppresses glucose production and increases lipid synthesis in
the liver. To understand the mechanisms for these seemingly paradoxical defects, we
examined the activation of atypical protein kinase C (aPKC) and protein kinase B (PKB), two
key signaling factors that operate downstream of phosphatidylinositol 3-kinase and regulate …
and hepatic overproduction of both glucose and lipids. These hepatic defects are perplexing
because insulin normally suppresses glucose production and increases lipid synthesis in
the liver. To understand the mechanisms for these seemingly paradoxical defects, we
examined the activation of atypical protein kinase C (aPKC) and protein kinase B (PKB), two
key signaling factors that operate downstream of phosphatidylinositol 3-kinase and regulate …