PMID- 27648697
OWN - NLM
STAT- MEDLINE
DCOM- 20180220
LR  - 20180302
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 47
IP  - 4
DP  - 2017 Apr
TI  - Interleukin-18 Reduces Blood Glucose and Modulates Plasma Corticosterone in a 
      Septic Mouse Model.
PG  - 455-462
LID - 10.1097/SHK.0000000000000747 [doi]
AB  - BACKGROUND: Dysregulation of glucose metabolism, including hyperglycemia with 
      insulin resistance, is commonly observed in critically ill patients. 
      Interleukin-18 (IL-18) improves the insulin resistance associated with obesity, 
      but the relationship between IL-18 and glucose metabolism in sepsis was unclear. 
      The purpose of this study was to investigate the influence of IL-18 on 
      hyperglycemia during sepsis. METHODS: Sepsis was induced using cecal ligation and 
      puncture (CLP) in wild-type (WT) mice, IL-18 knockout (KO) mice, and IL-18 KO 
      mice pretreated with recombinant IL-18. Blood glucose and plasma insulin, 
      glucagon, and corticosterone were measured. The mRNAs for gluconeogenic enzymes 
      (g6pc, pck1) and activation of insulin signaling were also analyzed. RESULTS: In 
      both WT and IL-18 KO mice, CLP operation led to hyperglycemia that lasted longer 
      (18 h) than after sham operation (6 h). Blood glucose levels in IL-18 KO mice 
      were significantly higher than in WT mice, without alteration of insulin or 
      glucagon levels. In IL-18 KO mice, insulin signaling in the liver and skeletal 
      muscle was decreased during hyperglycemia as compared with WT mice without 
      suppression of hepatic glucose production enzymes. Pretreatment with recombinant 
      IL-18 reduced blood glucose levels after CLP. Additionally, corticosterone levels 
      were higher after CLP in the presence of either endogenous or exogenous IL-18. 
      CONCLUSION: IL-18 may reduce blood glucose by modulating insulin signaling in the 
      liver during sepsis-induced hyperglycemia. IL-18 is an important factor 
      associated with alterations in blood glucose during sepsis.
FAU - Yamashita, Hayato
AU  - Yamashita H
AD  - *Department of Biophysics, Kobe University Graduate School of Health Sciences, 
      Hyogo, Japan daggerDepartment of Emergency, Disaster and Critical Care Medicine, Hyogo 
      College of Medicine, Hyogo, Japan double daggerDivision of Orthopedic Surgery, The Children's 
      Hospital of Philadelphia, Philadelphia, Pennsylvania.
FAU - Ishikawa, Michiko
AU  - Ishikawa M
FAU - Inoue, Taketo
AU  - Inoue T
FAU - Usami, Makoto
AU  - Usami M
FAU - Usami, Yu
AU  - Usami Y
FAU - Kotani, Joji
AU  - Kotani J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - 0 (Interleukin-18)
RN  - EC 3.1.3.9 (Glucose-6-Phosphatase)
RN  - EC 4.1.1.32 (Phosphoenolpyruvate Carboxykinase (GTP))
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Animals
MH  - Blood Glucose/*drug effects
MH  - Corticosterone/*blood
MH  - Disease Models, Animal
MH  - Glucose-6-Phosphatase/genetics
MH  - Insulin/blood
MH  - Interleukin-18/deficiency/genetics/*metabolism/*therapeutic use
MH  - Liver/drug effects/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Muscle, Skeletal/drug effects/metabolism
MH  - Phosphoenolpyruvate Carboxykinase (GTP)/genetics
MH  - Sepsis/*blood/drug therapy/metabolism
MH  - Signal Transduction/drug effects/genetics
EDAT- 2016/09/21 06:00
MHDA- 2018/02/21 06:00
CRDT- 2016/09/21 06:00
PHST- 2016/09/21 06:00 [pubmed]
PHST- 2018/02/21 06:00 [medline]
PHST- 2016/09/21 06:00 [entrez]
AID - 10.1097/SHK.0000000000000747 [doi]
PST - ppublish
SO  - Shock. 2017 Apr;47(4):455-462. doi: 10.1097/SHK.0000000000000747.