Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta - PubMed (original) (raw)

. 2001 Aug 31;293(5535):1673-7.

doi: 10.1126/science.1061620.

Affiliations

• PMID: 11533494
• DOI: 10.1126/science.1061620

Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta

M Yuan et al. Science. 2001.

Erratum in

• Science 2002 Jan 11;295(5553):277

Abstract

We show that high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing insulin signaling. Activation or overexpression of the IkappaB kinase beta (IKKbeta) attenuated insulin signaling in cultured cells, whereas IKKbeta inhibition reversed insulin resistance. Thus, IKKbeta, rather than the cyclooxygenases, appears to be the relevant molecular target. Heterozygous deletion (Ikkbeta+/-) protected against the development of insulin resistance during high-fat feeding and in obese Lep(ob/ob) mice. These findings implicate an inflammatory process in the pathogenesis of insulin resistance in obesity and type 2 diabetes mellitus and identify the IKKbeta pathway as a target for insulin sensitization.

PubMed Disclaimer

Publication types

MeSH terms

Substances

LinkOut - more resources

• Full Text Sources

  • Atypon
  • Ovid Technologies, Inc.

• Other Literature Sources

  • The Lens - Patent Citations Database

• Medical

  • MedlinePlus Health Information

• Molecular Biology Databases

  • Mouse Genome Informatics (MGI)

• Miscellaneous

  • NCI CPTAC Assay Portal