Diaphragm Acetylcholinesterase Multimeric Forms in Mice in Response to Burn Trauma

Tomera, John F.; Lilford, K.; Martyn, J. A. Jeevendra

doi:10.1097/00004630-199307000-00002

Cited by 2 publications

(1 citation statement)

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“…Each group consisted of 8 animals, unless otherwise indicated in the figure legends. Full-thickness third-degree burn injury comprising 12% of total body surface area was produced, as described previously [31]. Briefly, mice were treated by immersing the abdomen for 8 sec in 80°C water under anesthesia (pentobarbital sodium, 50 mg/kg BW, ip).…”

Section: Methodsmentioning

confidence: 99%

Inducible nitric oxide synthase deficiency ameliorates skeletal muscle insulin resistance but does not alter unexpected lower blood glucose levels after burn injury in C57BL/6 mice

Sugita

Kim

et al. 2012

Metabolism

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Objective Burn injury is associated with inflammatory responses and metabolic alterations including insulin resistance. Impaired insulin receptor substrate-1 (IRS-1)-mediated insulin signal transduction is a major component of insulin resistance in skeletal muscle following burn injury. To further investigate molecular mechanisms that underlie burn injury-induced insulin resistance, we study a role of inducible nitric oxide synthase (iNOS), a major mediator of inflammation, on burn-induced muscle insulin resistance in iNOS-deficient mice. Materials/Methods Full-thickness third-degree burn injury comprising 12% of total body surface area was produced in wild-type and iNOS-deficient C57BL/6 mice. Insulin-stimulated activation (phosphorylation) of insulin receptor (IR), IRS-1, and Akt was assessed by immunoblotting and immunoprecipitation. Insulin-stimulated glucose uptake by skeletal muscle was evaluated ex vivo. Results Burn injury caused induction of iNOS in skeletal muscle of wild-type mice. The increase of iNOS expression paralleled the increase of insulin resistance, as evidenced by decreased tyrosine phosphorylation of IR and IRS-1, IRS-1 expression, insulin-stimulated activation of phosphatidylinositol 3-kinase and Akt/PKB, and insulin-stimulated glucose uptake in mouse skeletal muscle. The absence of iNOS in genetically engineered mice significantly lessened burn injury-induced insulin resistance in skeletal muscle. In wild-type mice, insulin tolerance test revealed whole-body insulin resistance in burned mice compared to sham burned controls. This effect was reversed by iNOS deficiency. Unexpectedly, however, blood glucose levels were depressed in both wild-type and iNOS-deficient mice after burn injury. Conclusions Gene disruption of iNOS ameliorated the effect of burn on IRS-1-mediated insulin signaling in skeletal muscle of mice. These findings indicate that iNOS plays a significant role in burn injury-induced skeletal muscle insulin resistance.

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Section: Methodsmentioning

confidence: 99%