Effect of D-glucose feeding on mortality induced by sepsis.
10.4196/kjpp.2016.20.1.83
- Author:
Sung Su KIM
1
;
Yun Beom SIM
;
Soo Hyun PARK
;
Jae Ryeong LEE
;
Naveen SHARMA
;
Hong Won SUH
Author Information
1. Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University, Chuncheon 24252, Korea. hwsuh@hallym.ac.kr
- Publication Type:Original Article
- Keywords:
Blood glucose;
D-glucose;
PTX-sensitive G-proteins;
Sepsis-mortality;
Spinal cord
- MeSH:
Animals;
Blood Glucose;
Glucose*;
GTP-Binding Proteins;
Hyperglycemia;
Mice;
Mice, Inbred ICR;
Mortality*;
Pertussis Toxin;
Sepsis*;
Spinal Cord
- From:The Korean Journal of Physiology and Pharmacology
2016;20(1):83-89
- CountryRepublic of Korea
- Language:English
-
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 microg/5 ml) 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.
