Article
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 signaling patterns in liver versus muscle define phenotypes of type 2 diabetic and high fat-induced insulin-resistant states.
The Journal of biological chemistry - 11 Jun 2004
Standaert Mary L, Sajan Mini P, Miura Atsushi, Kanoh Yoshinori, Chen Hubert C, Farese Robert V, Farese Robert V
Abstract excerpt
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)...
Topics
- Animals
- Diabetes Mellitus, Type 2
- Dietary Fats
- Enzyme Activation
- Insulin
- Insulin Receptor Substrate Proteins
- Insulin Resistance
- Intracellular Signaling Peptides and Proteins