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Effect of D-glucose feeding on mortality induced by sepsis

  • Kim, Sung-Su (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University) ;
  • Sim, Yun-Beom (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University) ;
  • Park, Soo-Hyun (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University) ;
  • Lee, Jae-Ryeong (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University) ;
  • Sharma, Naveen (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University) ;
  • Suh, Hong-Won (Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University)
  • Received : 2015.09.12
  • Accepted : 2015.12.07
  • Published : 2016.01.01

Abstract

Sepsis is the life-threatening response to infection which can lead to tissue damage, organ failure, and death. In the current study, the effect of orally administered D-glucose on the mortality and the blood glucose level induced by D-Galactosamine (GaLN)/lipopolysaccharide (LPS)-induced sepsis was examined in ICR mice. After various amounts of D-glucose (from 1 to 8 g/kg) were orally fed, sepsis was induced by injecting intraperitoneally (i.p.) the mixture of GaLN /LPS. Oral pre-treatment with D-glucose dose-dependently increased the blood glucose level and caused a reduction of sepsis-induced mortality. The oral post-treatment with D-glucose (8 g/kg) up to 3 h caused an elevation of the blood glucose level and protected the mortality observed in sepsis model. However, D-glucose post-treated at 6, 9, or 12 h after sepsis induction did not affect the mortality and the blood glucose level induced by sepsis. Furthermore, the intrathecal (i.t.) pretreatment once with pertussis toxin (PTX; $0.1{\mu}g/5ml$) for 6 days caused a reduction of D-glucose-induced protection of mortality and hyperglycemia. Furthermore, once the hypoglycemic state is continued up to 6 h after sepsis initiated, sepsis-induced mortality could not be reversed by D-glucose fed orally. Based on these findings, it is assumed that the hypoglycemic duration between 3 and 6 h after the sepsis induction may be a critical time of period for the survival. D-glucose-induced protective effect against sepsis-induced mortality appears to be mediated via activating PTX-sensitive G-proteins in the spinal cord. Finally, the production of hyperglycemic state may be critical for the survival against the sepsis-induced mortality.

Keywords

References

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