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Exercise-induced endothelial progenitor cell mobilization is attenuated in impaired glucose tolerance and type 2 diabetes

Circulating endothelial progenitor cells (EPCs) contribute to vascular homeostasis and are fewer in those with type 2 diabetes mellitus (T2DM) compared with normal glucose tolerance (NGT), suggesting a link between EPCs and T2DM-associated vasculopathies. The purpose of this study was to assess EPC...

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Published in:Journal of applied physiology (1985) 2016-07, Vol.121 (1), p.36-41
Main Authors: Lutz, Andrew H, Blumenthal, Jacob B, Landers-Ramos, Rian Q, Prior, Steven J
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Blumenthal, Jacob B
Landers-Ramos, Rian Q
Prior, Steven J
description Circulating endothelial progenitor cells (EPCs) contribute to vascular homeostasis and are fewer in those with type 2 diabetes mellitus (T2DM) compared with normal glucose tolerance (NGT), suggesting a link between EPCs and T2DM-associated vasculopathies. The purpose of this study was to assess EPC number and mobilization by acute submaximal exercise in older adults with NGT, impaired glucose tolerance (IGT) or T2DM. We tested the hypothesis that EPC mobilization is lower in IGT compared with NGT and further reduced in older adults with T2DM. Forty-five older (50-75 yr of age) men and women with NGT (n = 18), IGT (n = 10), or T2DM (n = 17) were characterized and underwent submaximal aerobic exercise tests with blood sampling for enumeration of vascular endothelial growth factor receptor 2+ (VEGFR2+) cells, CD34+ hematopoetic progenitor cells, and CD34+/VEGFR2+ EPCs by flow cytometry before and after exercise. Basal EPC number was 65 and 61% lower in the IGT and T2DM groups, respectively, compared with the NGT group (P < 0.05). EPC number increased 23% after acute exercise in the NGT group (P < 0.01), but did not change in the IGT or T2DM groups. Before and after exercise, VEGFR2+ cell number was lower in a stepwise manner across the NGT, IGT, and T2DM groups (P < 0.05). Basal CD34+ cell number was lower in the IGT group compared with NGT (P < 0.05), but did not change after exercise in any group. These findings suggest a CD34+/VEGFR2+ EPC mobilization defect in IGT and T2DM that could play a role in the cardiovascular diseases and capillary rarefaction associated with insulin resistance.
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The purpose of this study was to assess EPC number and mobilization by acute submaximal exercise in older adults with NGT, impaired glucose tolerance (IGT) or T2DM. We tested the hypothesis that EPC mobilization is lower in IGT compared with NGT and further reduced in older adults with T2DM. Forty-five older (50-75 yr of age) men and women with NGT (n = 18), IGT (n = 10), or T2DM (n = 17) were characterized and underwent submaximal aerobic exercise tests with blood sampling for enumeration of vascular endothelial growth factor receptor 2+ (VEGFR2+) cells, CD34+ hematopoetic progenitor cells, and CD34+/VEGFR2+ EPCs by flow cytometry before and after exercise. Basal EPC number was 65 and 61% lower in the IGT and T2DM groups, respectively, compared with the NGT group (P &lt; 0.05). EPC number increased 23% after acute exercise in the NGT group (P &lt; 0.01), but did not change in the IGT or T2DM groups. 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source American Physiological Society Journals; American Physiological Society:Jisc Collections:American Physiological Society Journals ‘Read Publish & Join’ Agreement:2023-2024 (Reading list)
subjects Aged
Antigens, CD34 - metabolism
Blood Glucose - metabolism
Cardiovascular disease
Diabetes
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Endothelial Progenitor Cells - metabolism
Endothelial Progenitor Cells - physiology
Endothelium
Exercise
Exercise - physiology
Female
Glucose - metabolism
Glucose Intolerance - metabolism
Glucose Intolerance - physiopathology
Glucose Tolerance Test - methods
Homeostasis
Humans
Insulin - metabolism
Insulin resistance
Insulin Resistance - physiology
Male
Middle Aged
Vascular endothelial growth factor
Vascular Endothelial Growth Factor Receptor-2 - metabolism
title Exercise-induced endothelial progenitor cell mobilization is attenuated in impaired glucose tolerance and type 2 diabetes
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