Insulin therapy for hyperglycemia in neonatal sepsis using a preterm mouse model
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Abstract
Background Stress-induced hyperglycemia is a frequent complication of neonatal sepsis. Hyperglycemia induces oxidative stress and immunosuppression. We investigated the glucose kinetics and effect of insulin administration during stress-induced hyperglycemia in a neonatal sepsis mouse model. Methods A stock cecal slurry (CS) solution was prepared from adult cecums and 3.0 mg of CS/g (LD40) was administered intraperitoneally to 4-day-old FVB mouse pups. Blood glucose levels were measured at 1.5, 3, 6, and 9 h post-sepsis induction and compared with basal levels. Two different doses of ultrafast-acting insulin were administered subcutaneously, and blood glucose levels and survival rates were monitored. Results Blood glucose levels were significantly higher than those of baseline levels with a peak at 3 h, which progressively decreased from 6 to 9 h post-sepsis induction. Insulin treatment reduced post-sepsis-induced hyperglycemia at 1.5 and 3 h. The mortality rate of CS-only pups (39%) was similar to that of CS + 1 U/kg insulin pups (60%). However, the mortality rate of CS + 5 U/kg insulin pups (82%) was significantly higher than that of CS-only pups. Conclusions Marked hyperglycemia was induced immediately after post-sepsis induction, and the high-dose insulin treatment increased mortality post-induction. Stress-induced hyperglycemia could therefore be a physiological and protective response for preterm sepsis, and aggressive treatment of this hyperglycemia might be contraindicated.
Journal
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- Pediatrics International
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Pediatrics International 62 (5), 581-586, 2020-05
Wiley
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Details 詳細情報について
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- CRID
- 1050856995322495488
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- NII Article ID
- 120006864552
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- NII Book ID
- AA11631585
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- ISSN
- 1442200X
- 13288067
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- HANDLE
- 20.500.14094/90007175
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- Text Lang
- en
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- Article Type
- journal article
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- Data Source
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- IRDB
- Crossref
- CiNii Articles
- KAKEN