Targeted disruption of inducible nitric oxide synthase protects against aging, S-nitrosation, and insulin resistance in muscle of male mice

Diabetes. 2013 Feb;62(2):466-70. doi: 10.2337/db12-0339. Epub 2012 Sep 18.

Abstract

Accumulating evidence has demonstrated that S-nitrosation of proteins plays a critical role in several human diseases. Here, we explored the role of inducible nitric oxide synthase (iNOS) in the S-nitrosation of proteins involved in the early steps of the insulin-signaling pathway and insulin resistance in the skeletal muscle of aged mice. Aging increased iNOS expression and S-nitrosation of major proteins involved in insulin signaling, thereby reducing insulin sensitivity in skeletal muscle. Conversely, aged iNOS-null mice were protected from S-nitrosation-induced insulin resistance. Moreover, pharmacological treatment with an iNOS inhibitor and acute exercise reduced iNOS-induced S-nitrosation and increased insulin sensitivity in the muscle of aged animals. These findings indicate that the insulin resistance observed in aged mice is mainly mediated through the S-nitrosation of the insulin-signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / drug effects
  • Aging / metabolism*
  • Animals
  • Enzyme Inhibitors / pharmacology
  • Insulin / metabolism
  • Insulin Resistance / physiology*
  • Lysine / analogs & derivatives
  • Lysine / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / enzymology*
  • Nitric Oxide Synthase Type II / antagonists & inhibitors
  • Nitric Oxide Synthase Type II / metabolism*
  • Nitrosation
  • Physical Conditioning, Animal
  • Signal Transduction / drug effects
  • Signal Transduction / physiology

Substances

  • Enzyme Inhibitors
  • Insulin
  • N(6)-(1-iminoethyl)lysine
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Lysine