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Effect of D-glucose feeding on mortality induced by sepsis

机译:D-葡萄糖喂养对败血症诱导的死亡率的影响

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摘要

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 µg/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.
机译:败血症是对感染的威胁生命的反应,可导致组织损伤,器官衰竭和死亡。在当前的研究中,在ICR小鼠中检查了口服D-葡萄糖对D-半乳糖胺(GaLN)/脂多糖(LPS)引起的败血症诱导的死亡率和血糖水平的影响。口服喂食各种量的D-葡萄糖(1至8 g / kg)后,通过腹膜内(i.p.)注射GaLN / LPS混合物诱导败血症。口服D-葡萄糖预处理可以剂量依赖性地增加血糖水平,并降低败血症诱导的死亡率。口服D-葡萄糖(8 g / kg)进行长达3小时的后处理可导致血糖水平升高并保护败血症模型中观察到的死亡率。然而,在败血症诱导后6、9或12小时后处理的D-葡萄糖不影响败血症诱导的死亡率和血糖水平。此外,鞘内(i.t.)一次用百日咳毒素(PTX; 0.1 µg / 5 ml)预处理6天导致D-葡萄糖诱导的对死亡和高血糖症的保护作用降低。此外,一旦脓毒症发作后低血糖状态持续至6小时,口服D-葡萄糖不能逆转败血症诱导的死亡率。基于这些发现,可以认为败血症诱导后3至6 h的降血糖持续时间可能是生存期的关键时间。 D-葡萄糖诱导的抗败血症诱导的死亡的保护作用似乎是通过激活脊髓中PTX敏感的G蛋白来介导的。最后,高血糖状态的产生对于败血症诱导的死亡率的存活可能至关重要。

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