Acetoacetate increases expression of intercellular adhesion molecule-1 (ICAM-1) in human brain microvascular endothelial cells

William H. Hoffman, Charles Cheng, Gregory G Passmore, James Edwin Carroll, David C Hess

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

It has been hypothesized that ketone bodies cause activation of brain endothelial cells and that this is a factor in the intracerebral crises of diabetic ketoacidosis (DKA). In this study we used cultured human brain microvascular endothelial cells (HBMEC) to investigate the effect of beta hydroxybutyrate (BOHB) and acetoacetate (AcAc) on the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1). Increasing concentrations of AcAc, but not BOHB, caused a significant upregulation of ICAM-1 in comparison to unstimulated cells. Glucose concentrations of 10 and 30 mM, but not 50 mM, also resulted in increased expression of ICAM-1. These results support the hypothesis that activation of HBMEC is involved in the acute complications of DKA, and that ketone bodies and hyperglycemia are factors in the perturbed membrane function.

Original languageEnglish (US)
Pages (from-to)71-74
Number of pages4
JournalNeuroscience Letters
Volume334
Issue number2
DOIs
StatePublished - Dec 13 2002

Fingerprint

Intercellular Adhesion Molecule-1
Ketone Bodies
Diabetic Ketoacidosis
Endothelial Cells
Brain
3-Hydroxybutyric Acid
Hyperglycemia
Up-Regulation
Glucose
Membranes
acetoacetic acid

Keywords

  • Glucose
  • Human brain
  • Intercellular adhesion molecule-1

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

@article{d4fe0eece9d94c8993da089f3e05e8c4,
title = "Acetoacetate increases expression of intercellular adhesion molecule-1 (ICAM-1) in human brain microvascular endothelial cells",
abstract = "It has been hypothesized that ketone bodies cause activation of brain endothelial cells and that this is a factor in the intracerebral crises of diabetic ketoacidosis (DKA). In this study we used cultured human brain microvascular endothelial cells (HBMEC) to investigate the effect of beta hydroxybutyrate (BOHB) and acetoacetate (AcAc) on the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1). Increasing concentrations of AcAc, but not BOHB, caused a significant upregulation of ICAM-1 in comparison to unstimulated cells. Glucose concentrations of 10 and 30 mM, but not 50 mM, also resulted in increased expression of ICAM-1. These results support the hypothesis that activation of HBMEC is involved in the acute complications of DKA, and that ketone bodies and hyperglycemia are factors in the perturbed membrane function.",
keywords = "Glucose, Human brain, Intercellular adhesion molecule-1",
author = "Hoffman, {William H.} and Charles Cheng and Passmore, {Gregory G} and Carroll, {James Edwin} and Hess, {David C}",
year = "2002",
month = "12",
day = "13",
doi = "10.1016/S0304-3940(02)00816-9",
language = "English (US)",
volume = "334",
pages = "71--74",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Acetoacetate increases expression of intercellular adhesion molecule-1 (ICAM-1) in human brain microvascular endothelial cells

AU - Hoffman, William H.

AU - Cheng, Charles

AU - Passmore, Gregory G

AU - Carroll, James Edwin

AU - Hess, David C

PY - 2002/12/13

Y1 - 2002/12/13

N2 - It has been hypothesized that ketone bodies cause activation of brain endothelial cells and that this is a factor in the intracerebral crises of diabetic ketoacidosis (DKA). In this study we used cultured human brain microvascular endothelial cells (HBMEC) to investigate the effect of beta hydroxybutyrate (BOHB) and acetoacetate (AcAc) on the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1). Increasing concentrations of AcAc, but not BOHB, caused a significant upregulation of ICAM-1 in comparison to unstimulated cells. Glucose concentrations of 10 and 30 mM, but not 50 mM, also resulted in increased expression of ICAM-1. These results support the hypothesis that activation of HBMEC is involved in the acute complications of DKA, and that ketone bodies and hyperglycemia are factors in the perturbed membrane function.

AB - It has been hypothesized that ketone bodies cause activation of brain endothelial cells and that this is a factor in the intracerebral crises of diabetic ketoacidosis (DKA). In this study we used cultured human brain microvascular endothelial cells (HBMEC) to investigate the effect of beta hydroxybutyrate (BOHB) and acetoacetate (AcAc) on the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1). Increasing concentrations of AcAc, but not BOHB, caused a significant upregulation of ICAM-1 in comparison to unstimulated cells. Glucose concentrations of 10 and 30 mM, but not 50 mM, also resulted in increased expression of ICAM-1. These results support the hypothesis that activation of HBMEC is involved in the acute complications of DKA, and that ketone bodies and hyperglycemia are factors in the perturbed membrane function.

KW - Glucose

KW - Human brain

KW - Intercellular adhesion molecule-1

UR - http://www.scopus.com/inward/record.url?scp=0037073574&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037073574&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(02)00816-9

DO - 10.1016/S0304-3940(02)00816-9

M3 - Article

VL - 334

SP - 71

EP - 74

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 2

ER -