Propranolol improves impaired hepatic phosphatidylinositol 3-kinase/akt signaling after burn injury.

Natasha C. Brooks, Juquan Song, Darren Boehning, Robert Kraft, Celeste C. Finnerty, David Herndon, Marc G. Jeschke

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Severe burn injury is associated with induction of the hepatic endoplasmic reticulum (ER) stress response. ER stress leads to activation of c-Jun N-terminal kinase (JNK), suppression of insulin receptor signaling via phosphorylation of insulin receptor substrate 1 and subsequent insulin resistance. Marked and sustained increases in catecholamines are prominent after a burn. Here, we show that administration of propranolol, a nonselective β1/2 adrenergic receptor antagonist, attenuates ER stress and JNK activation. Attenuation of ER stress by propranolol results in increased insulin sensitivity, as determined by activation of hepatic phosphatidylinositol 3-kinase and Akt. We conclude that catecholamine release is responsible for the ER stress response and impaired insulin receptor signaling after burn injury.

Original languageEnglish (US)
Pages (from-to)707-711
Number of pages5
JournalMolecular medicine (Cambridge, Mass.)
StatePublished - 2012

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Genetics(clinical)


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