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Related Experiment Videos

Lipopolysaccharide Potentiates Insulin-Driven Hypoglycemic Shock.

Jon A Hagar1,2,3, Matthew L Edin4, Fred B Lih4

  • 1Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.

Journal of Immunology (Baltimore, Md. : 1950)
|October 18, 2017
PubMed
Summary

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Intensive insulin therapy (IIT) can cause hypoglycemia in septic patients. Lipopolysaccharide (LPS) impairs insulin clearance and amplifies insulin signaling, increasing hypoglycemia risk during sepsis.

Area of Science:

  • Biomedical Science
  • Endocrinology
  • Immunology

Background:

  • Critically ill patients often have hyperglycemia.
  • Conventional insulin therapy improves survival.
  • Intensive insulin therapy (IIT) targeting normal glucose levels increases hypoglycemia and mortality, especially in septic patients.

Purpose of the Study:

  • To investigate the mechanism of IIT-induced hypoglycemia in sepsis.
  • To determine if impaired insulin clearance contributes to hypoglycemia in septic patients.

Main Methods:

  • Mice were administered insulin and lipopolysaccharide (LPS).
  • Insulin clearance, insulin receptor signaling, and inflammatory mediators were assessed.
  • A sepsis animal model using Salmonella typhimurium infection was employed.

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Main Results:

  • Codelivery of insulin and LPS induced rapid hypoglycemic shock in mice.
  • LPS impaired insulin clearance and amplified insulin receptor signaling.
  • Caspase-11, TLR4, and complement mediated these effects via eicosanoid production.
  • Sepsis model mice showed impaired insulin clearance and insulin resistance.

Conclusions:

  • Impaired insulin clearance may explain increased hypoglycemia susceptibility in septic patients during IIT.
  • IIT may be contraindicated in septic patients due to increased hypoglycemia risk.