Diabetic ketoacidosis induces in vivo activation of human T-lymphocytes

Diabetic ketoacidosis (DKA) is an inflammatory state associated with immune responses in polymorphonuclear cells (PMN). Activation of subgroup of T-lymphocytes in PMN of DKA patients, however, is not known. We studied in vivo activation of CD4 and CD8 lymphocytes by measuring de novo growth factor r...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-03, Vol.315 (2), p.404-407
Main Authors: Kitabchi, Abbas E, Stentz, Frankie B, Umpierrez, Guillermo E
Format: Article
Language:English
Subjects:
CD4
CD4-Positive T-Lymphocytes - metabolism
CD8 T-lymphocytes
CD8-Positive T-Lymphocytes - metabolism
Cytokines
Diabetic Ketoacidosis - blood
Diabetic Ketoacidosis - pathology
DKA
Dose-Response Relationship, Drug
Flow Cytometry
Fluoresceins - pharmacology
Growth factor receptors
Growth Substances - metabolism
Humans
Insulin-Like Growth Factor I - metabolism
Interleukin-2 - metabolism
Lipid peroxidation
Lymphocyte Activation
Lymphocytes - metabolism
Models, Biological
Oxidative Stress
Reactive Oxygen Species
T-Lymphocytes - metabolism
TBA
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Diabetic ketoacidosis (DKA) is an inflammatory state associated with immune responses in polymorphonuclear cells (PMN). Activation of subgroup of T-lymphocytes in PMN of DKA patients, however, is not known. We studied in vivo activation of CD4 and CD8 lymphocytes by measuring de novo growth factor receptor for insulin, IGF-1, and IL-2 in eight patients on admission and at resolution of DKA, and compared them with matched controls. The presence of these receptors was demonstrated in all patients’ lymphocytes on admission, but not in control subjects. This event was associated with increased levels of thiobarbituric acid-reacting material and dichlorofluorescien, as markers of oxidative stress. Based on these new findings and works in the literature, we hypothesize that hyperglycemia/ketosis results in increased reactive oxygen species, leading to increased levels of cytokines and emergence of growth factor receptors. We propose DKA changes the T-lymphocytes to insulin sensitive tissues as a compensatory mechanism.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2004.01.065