Peptide VSAK maintains tissue glucose uptake and attenuates pro-inflammatory responses caused by LPS in an experimental model of the systemic inflammatory response syndrome: a PET study

Sci Rep. 2021 Jul 20;11(1):14752. doi: 10.1038/s41598-021-94224-2.

Abstract

The present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS). Animals concomitantly treated with lipopolysaccharides (LPS) and peptide VSAK show important protection in the loss of radiolabeled-glucose uptake observed in diverse organs when animals are exclusively treated with LPS. Treatment with peptide VSAK prevented the onset of changes in serum levels of glucose and insulin associated with the establishment of SIRS and the insulin resistance-like syndrome. Treatment with peptide VSAK also allowed an important attenuation in the circulating levels of pro-inflammatory molecules in LPS-treated animals. As a whole, our data suggest that peptide VSAK might be considered as a candidate in the development of new therapeutic possibilities focused on mitigating the harmful effects produced by lipopolysaccharides during the course of SIRS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Disease Models, Animal
  • Fluorodeoxyglucose F18 / chemistry
  • Glucose / analysis
  • Glucose / metabolism*
  • Insulin / blood
  • Interleukin-1beta / blood
  • Kidney / diagnostic imaging
  • Kidney / metabolism
  • Lipid Bilayers / chemistry
  • Lipid Bilayers / metabolism
  • Lipopolysaccharides / administration & dosage*
  • Lipopolysaccharides / metabolism
  • Liver / diagnostic imaging
  • Liver / metabolism
  • Male
  • Molecular Dynamics Simulation
  • Peptides / administration & dosage*
  • Peptides / chemistry
  • Peptides / metabolism
  • Positron-Emission Tomography*
  • Rabbits
  • Systemic Inflammatory Response Syndrome / metabolism
  • Systemic Inflammatory Response Syndrome / pathology*
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Insulin
  • Interleukin-1beta
  • Lipid Bilayers
  • Lipopolysaccharides
  • Peptides
  • Tumor Necrosis Factor-alpha
  • Fluorodeoxyglucose F18
  • Glucose