J 2008

THE EFFECT OF SUPEROXIDE DISMUTASE OVEREXPRESSION ON HEPATIC GLUCONEOGENESIS AND WHOLE-BODY GLUCOSE OXIDATION DURING RESUSCITATED NORMOTENSIVE MURINE SEPTIC SHOCK.

ŠIMKOVÁ, Vladislava, Katja BAUMGART, Josef VOGT, Ulrich WACHTER, Sandra WEBER et. al.

Základní údaje

Originální název

THE EFFECT OF SUPEROXIDE DISMUTASE OVEREXPRESSION ON HEPATIC GLUCONEOGENESIS AND WHOLE-BODY GLUCOSE OXIDATION DURING RESUSCITATED NORMOTENSIVE MURINE SEPTIC SHOCK.

Název anglicky

THE EFFECT OF SUPEROXIDE DISMUTASE OVEREXPRESSION ON HEPATIC GLUCONEOGENESIS AND WHOLE-BODY GLUCOSE OXIDATION DURING RESUSCITATED NORMOTENSIVE MURINE SEPTIC SHOCK.

Autoři

ŠIMKOVÁ, Vladislava, Katja BAUMGART, Josef VOGT, Ulrich WACHTER, Sandra WEBER, Michael GRÖGER, Günter SPEIT, Peter RADERMACHER, Gerd ALBUSZIES a Eberhad BARTH

Vydání

Shock, 2008, 1073-2322

Další údaje

Typ výsledku

Článek v odborném periodiku

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 3.394

Organizační jednotka

Lékařská fakulta

Příznaky

Mezinárodní význam
Změněno: 18. 4. 2008 09:05, MUDr. Vladislava Šimková, Ph.D.

Anotace

ORIG EN

V originále

Besides excess cytokine and NO production, enhanced oxygen radical formation was referred to contribute to the impaired hepatic gluconeogenesis during sepsis or endotoxemia. Therefore, we tested the hypothesis that genetic overexpression of the Cu/Zn-superoxide dismutase (SOD-1) may restore the sepsis-related lack of the norepinephrine-induced increase in hepatic gluconeogenesis and whole-body glucose oxidation. Anesthetized, ventilated, and instrumented wild-type control, and heterozygous and homozygous SOD-1-overexpressing mice received hydroxyethyl starch and norepinephrine to maintain normotensive hemodynamics measured at 18, 21, and 24 h after cecal ligation and puncture (CLP) or sham operation. Hepatic gluconeogenesis and whole-body glucose oxidation were calculated from liver tissue isotope and expiratory CO2 enrichments during continuous i.v. 1,2,3,4,5,6-C6-glucose. Superior mesenteric artery and portal vein flows (ultrasound flow probes) and hepatic microcirculatory perfusion (Laser Doppler flowmetry) and O2 saturation (remission spectrophotometry) were comparable in the CLP and sham-operated animals, without any difference related to the mouse strain. Despite continuous i.v. norepinephrine necessary in the CLP mice, both glycemia and hepatic gluconeogenesis were similar, irrespective of the presence of sepsis and the genetic strain. Glucose oxidation rate progressively increased in the CLP groups, again without difference between the genetic strains. The surgery- and CLP-induced increase in liver cell oxidative DNA damage (tail moment in the comet assay) was less pronounced in the homozygous mice. Heterozygous nor homozygous SOD-1 overexpression did not improve the sepsis-related impairment of carbohydrate metabolism, possibly because of the lacking increase of the tissue catalase and the mitochondrial SOD activity, and the ongoing i.v. norepinephrine

Anglicky

Besides excess cytokine and NO production, enhanced oxygen radical formation was referred to contribute to the impaired hepatic gluconeogenesis during sepsis or endotoxemia. Therefore, we tested the hypothesis that genetic overexpression of the Cu/Zn-superoxide dismutase (SOD-1) may restore the sepsis-related lack of the norepinephrine-induced increase in hepatic gluconeogenesis and whole-body glucose oxidation. Anesthetized, ventilated, and instrumented wild-type control, and heterozygous and homozygous SOD-1-overexpressing mice received hydroxyethyl starch and norepinephrine to maintain normotensive hemodynamics measured at 18, 21, and 24 h after cecal ligation and puncture (CLP) or sham operation. Hepatic gluconeogenesis and whole-body glucose oxidation were calculated from liver tissue isotope and expiratory CO2 enrichments during continuous i.v. 1,2,3,4,5,6-C6-glucose. Superior mesenteric artery and portal vein flows (ultrasound flow probes) and hepatic microcirculatory perfusion (Laser Doppler flowmetry) and O2 saturation (remission spectrophotometry) were comparable in the CLP and sham-operated animals, without any difference related to the mouse strain. Despite continuous i.v. norepinephrine necessary in the CLP mice, both glycemia and hepatic gluconeogenesis were similar, irrespective of the presence of sepsis and the genetic strain. Glucose oxidation rate progressively increased in the CLP groups, again without difference between the genetic strains. The surgery- and CLP-induced increase in liver cell oxidative DNA damage (tail moment in the comet assay) was less pronounced in the homozygous mice. Heterozygous nor homozygous SOD-1 overexpression did not improve the sepsis-related impairment of carbohydrate metabolism, possibly because of the lacking increase of the tissue catalase and the mitochondrial SOD activity, and the ongoing i.v. norepinephrine