Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice

Hayato Yamashita, Michiko Aoyama-Ishikawa, Miki Takahara, Chisato Yamauchi, Taketo Inoue, Makoto Miyoshi, Noriaki Maeshige, Makoto Usami, Atsunori Nakao, Joji Kotani

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: Hyperglycemia associated with insulin resistance is common among critically ill patients. Interleukin (IL)-18 has been linked with hyperglycemia and insulin resistance in chronic disease, but the relation between IL-18 and insulin resistance during critical illness was unexplored. This study investigated whether IL-18 modulates hyperglycemia and insulin resistance during acute inflammation. Methods: We injected lipopolysaccharide (LPS) 40 mg/kg into wild-type (WT) and IL-18 knockout (KO) mice to induce endotoxemia and examined insulin resistance and insulin-dependent signaling pathways during the acute phase. Results: During the first hour after LPS treatment, IL-18 KO mice showed higher blood glucose and insulin and less insulin receptor substrate-1 and less phosphorylated Akt in the liver compared with WT mice. Interleukin-18 KO mice exhibited better survival after LPS treatment. Conclusions: The findings suggest that endogenous IL-18 may attenuate hyperglycemia and modulate insulin signaling in liver. Accordingly, IL-18 may modulate glucose tolerance during acute inflammation.

Original languageEnglish
Pages (from-to)90-96
Number of pages7
JournalSurgical Infections
Volume16
Issue number1
DOIs
Publication statusPublished - Feb 1 2015
Externally publishedYes

Fingerprint

Interleukin-18
Endotoxemia
Hyperinsulinism
Hyperglycemia
Insulin Resistance
Knockout Mice
Lipopolysaccharides
Insulin
Critical Illness
Inflammation
Insulin Receptor Substrate Proteins
Liver
Blood Glucose
Chronic Disease
Glucose
Survival
Therapeutics

ASJC Scopus subject areas

  • Surgery
  • Infectious Diseases
  • Microbiology (medical)
  • Medicine(all)

Cite this

Yamashita, H., Aoyama-Ishikawa, M., Takahara, M., Yamauchi, C., Inoue, T., Miyoshi, M., ... Kotani, J. (2015). Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice. Surgical Infections, 16(1), 90-96. https://doi.org/10.1089/sur.2013.269

Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice. / Yamashita, Hayato; Aoyama-Ishikawa, Michiko; Takahara, Miki; Yamauchi, Chisato; Inoue, Taketo; Miyoshi, Makoto; Maeshige, Noriaki; Usami, Makoto; Nakao, Atsunori; Kotani, Joji.

In: Surgical Infections, Vol. 16, No. 1, 01.02.2015, p. 90-96.

Research output: Contribution to journalArticle

Yamashita, H, Aoyama-Ishikawa, M, Takahara, M, Yamauchi, C, Inoue, T, Miyoshi, M, Maeshige, N, Usami, M, Nakao, A & Kotani, J 2015, 'Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice', Surgical Infections, vol. 16, no. 1, pp. 90-96. https://doi.org/10.1089/sur.2013.269
Yamashita, Hayato ; Aoyama-Ishikawa, Michiko ; Takahara, Miki ; Yamauchi, Chisato ; Inoue, Taketo ; Miyoshi, Makoto ; Maeshige, Noriaki ; Usami, Makoto ; Nakao, Atsunori ; Kotani, Joji. / Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice. In: Surgical Infections. 2015 ; Vol. 16, No. 1. pp. 90-96.
@article{4592f2f0bc224b5394802da8bc5ea4bc,
title = "Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice",
abstract = "Background: Hyperglycemia associated with insulin resistance is common among critically ill patients. Interleukin (IL)-18 has been linked with hyperglycemia and insulin resistance in chronic disease, but the relation between IL-18 and insulin resistance during critical illness was unexplored. This study investigated whether IL-18 modulates hyperglycemia and insulin resistance during acute inflammation. Methods: We injected lipopolysaccharide (LPS) 40 mg/kg into wild-type (WT) and IL-18 knockout (KO) mice to induce endotoxemia and examined insulin resistance and insulin-dependent signaling pathways during the acute phase. Results: During the first hour after LPS treatment, IL-18 KO mice showed higher blood glucose and insulin and less insulin receptor substrate-1 and less phosphorylated Akt in the liver compared with WT mice. Interleukin-18 KO mice exhibited better survival after LPS treatment. Conclusions: The findings suggest that endogenous IL-18 may attenuate hyperglycemia and modulate insulin signaling in liver. Accordingly, IL-18 may modulate glucose tolerance during acute inflammation.",
author = "Hayato Yamashita and Michiko Aoyama-Ishikawa and Miki Takahara and Chisato Yamauchi and Taketo Inoue and Makoto Miyoshi and Noriaki Maeshige and Makoto Usami and Atsunori Nakao and Joji Kotani",
year = "2015",
month = "2",
day = "1",
doi = "10.1089/sur.2013.269",
language = "English",
volume = "16",
pages = "90--96",
journal = "Surgical Infections",
issn = "1096-2964",
publisher = "Mary Ann Liebert Inc.",
number = "1",

}

TY - JOUR

T1 - Endogenous Interleukin 18 Suppresses Hyperglycemia and Hyperinsulinemia during the Acute Phase of Endotoxemia in Mice

AU - Yamashita, Hayato

AU - Aoyama-Ishikawa, Michiko

AU - Takahara, Miki

AU - Yamauchi, Chisato

AU - Inoue, Taketo

AU - Miyoshi, Makoto

AU - Maeshige, Noriaki

AU - Usami, Makoto

AU - Nakao, Atsunori

AU - Kotani, Joji

PY - 2015/2/1

Y1 - 2015/2/1

N2 - Background: Hyperglycemia associated with insulin resistance is common among critically ill patients. Interleukin (IL)-18 has been linked with hyperglycemia and insulin resistance in chronic disease, but the relation between IL-18 and insulin resistance during critical illness was unexplored. This study investigated whether IL-18 modulates hyperglycemia and insulin resistance during acute inflammation. Methods: We injected lipopolysaccharide (LPS) 40 mg/kg into wild-type (WT) and IL-18 knockout (KO) mice to induce endotoxemia and examined insulin resistance and insulin-dependent signaling pathways during the acute phase. Results: During the first hour after LPS treatment, IL-18 KO mice showed higher blood glucose and insulin and less insulin receptor substrate-1 and less phosphorylated Akt in the liver compared with WT mice. Interleukin-18 KO mice exhibited better survival after LPS treatment. Conclusions: The findings suggest that endogenous IL-18 may attenuate hyperglycemia and modulate insulin signaling in liver. Accordingly, IL-18 may modulate glucose tolerance during acute inflammation.

AB - Background: Hyperglycemia associated with insulin resistance is common among critically ill patients. Interleukin (IL)-18 has been linked with hyperglycemia and insulin resistance in chronic disease, but the relation between IL-18 and insulin resistance during critical illness was unexplored. This study investigated whether IL-18 modulates hyperglycemia and insulin resistance during acute inflammation. Methods: We injected lipopolysaccharide (LPS) 40 mg/kg into wild-type (WT) and IL-18 knockout (KO) mice to induce endotoxemia and examined insulin resistance and insulin-dependent signaling pathways during the acute phase. Results: During the first hour after LPS treatment, IL-18 KO mice showed higher blood glucose and insulin and less insulin receptor substrate-1 and less phosphorylated Akt in the liver compared with WT mice. Interleukin-18 KO mice exhibited better survival after LPS treatment. Conclusions: The findings suggest that endogenous IL-18 may attenuate hyperglycemia and modulate insulin signaling in liver. Accordingly, IL-18 may modulate glucose tolerance during acute inflammation.

UR - http://www.scopus.com/inward/record.url?scp=84924975553&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84924975553&partnerID=8YFLogxK

U2 - 10.1089/sur.2013.269

DO - 10.1089/sur.2013.269

M3 - Article

C2 - 25651466

AN - SCOPUS:84924975553

VL - 16

SP - 90

EP - 96

JO - Surgical Infections

JF - Surgical Infections

SN - 1096-2964

IS - 1

ER -