Circulating levels of mitochondrial uncoupling protein 2, but not prohibitin, are lower in humans with type 2 diabetes and correlate with brachial artery flow-mediated dilation.
Adult
Aged
Biomarkers
/ blood
Brachial Artery
/ diagnostic imaging
Case-Control Studies
Diabetes Mellitus, Type 2
/ blood
Female
Humans
Leukocytes
/ metabolism
Male
Membrane Potential, Mitochondrial
Middle Aged
Mitochondria
/ metabolism
Pilot Projects
Prohibitins
Repressor Proteins
/ blood
Uncoupling Protein 2
/ blood
Vasodilation
Endothelium
Mitochondria
Mitochondrial membrane potential
PHB
UCP2
Journal
Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637
Informations de publication
Date de publication:
09 11 2019
09 11 2019
Historique:
received:
25
07
2019
accepted:
28
10
2019
entrez:
11
11
2019
pubmed:
11
11
2019
medline:
27
5
2020
Statut:
epublish
Résumé
Excessive reactive oxygen species from endothelial mitochondria in type 2 diabetes individuals (T2DM) may occur through multiple related mechanisms, including production of mitochondrial reactive oxygen species (mtROS), inner mitochondrial membrane (Δψ Plasma samples and data from a total of 107 individuals with (N = 52) and without T2DM (N = 55) were included in this study. Brachial artery flow mediated dilation (FMD) was measured by ultrasound. ELISA was performed to measure serum concentrations of PHB1 and UCP2. Mitochondrial membrane potential was measured from isolated leukocytes using JC-1 dye. Serum UCP2 levels were significantly lower in T2DM subjects compared to control subjects (3.01 ± 0.34 vs. 4.11 ± 0.41 ng/mL, P = 0.04). There were no significant differences in levels of serum PHB. UCP2 levels significantly and positively correlated with FMDmm (r = 0.30, P = 0.03) in T2DM subjects only and remained significant after multivariable adjustment. Within T2DM subjects, serum PHB levels were significantly and negatively correlated with UCP2 levels (ρ = - 0.35, P = 0.03). Circulating UCP2 levels are lower in T2DM patients and correlate with endothelium-dependent vasodilation in conduit vessels. UCP2 could be biomarker surrogate for overall vascular health in patients with T2DM and merits additional investigation.
Sections du résumé
BACKGROUND
Excessive reactive oxygen species from endothelial mitochondria in type 2 diabetes individuals (T2DM) may occur through multiple related mechanisms, including production of mitochondrial reactive oxygen species (mtROS), inner mitochondrial membrane (Δψ
METHODS
Plasma samples and data from a total of 107 individuals with (N = 52) and without T2DM (N = 55) were included in this study. Brachial artery flow mediated dilation (FMD) was measured by ultrasound. ELISA was performed to measure serum concentrations of PHB1 and UCP2. Mitochondrial membrane potential was measured from isolated leukocytes using JC-1 dye.
RESULTS
Serum UCP2 levels were significantly lower in T2DM subjects compared to control subjects (3.01 ± 0.34 vs. 4.11 ± 0.41 ng/mL, P = 0.04). There were no significant differences in levels of serum PHB. UCP2 levels significantly and positively correlated with FMDmm (r = 0.30, P = 0.03) in T2DM subjects only and remained significant after multivariable adjustment. Within T2DM subjects, serum PHB levels were significantly and negatively correlated with UCP2 levels (ρ = - 0.35, P = 0.03).
CONCLUSION
Circulating UCP2 levels are lower in T2DM patients and correlate with endothelium-dependent vasodilation in conduit vessels. UCP2 could be biomarker surrogate for overall vascular health in patients with T2DM and merits additional investigation.
Identifiants
pubmed: 31706320
doi: 10.1186/s12933-019-0956-4
pii: 10.1186/s12933-019-0956-4
pmc: PMC6842161
doi:
Substances chimiques
Biomarkers
0
PHB protein, human
0
Prohibitins
0
Repressor Proteins
0
UCP2 protein, human
0
Uncoupling Protein 2
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
148Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL128240
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL144098
Pays : United States
Organisme : NHLBI NIH HHS
ID : R38 HL143561
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM089586
Pays : United States
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