Suppr超能文献

运动诱导的内皮祖细胞动员在糖耐量受损和2型糖尿病中减弱。

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

作者信息

Lutz Andrew H, Blumenthal Jacob B, Landers-Ramos Rian Q, Prior Steven J

机构信息

Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Maryland School of Medicine and the Baltimore Veterans Affairs Geriatric Research, Education and Clinical Center, Baltimore, Maryland.

Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Maryland School of Medicine and the Baltimore Veterans Affairs Geriatric Research, Education and Clinical Center, Baltimore, Maryland

出版信息

J Appl Physiol (1985). 2016 Jul 1;121(1):36-41. doi: 10.1152/japplphysiol.00349.2016. Epub 2016 May 19.

Abstract

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.

摘要

循环内皮祖细胞(EPCs)有助于维持血管稳态,与糖耐量正常(NGT)者相比,2型糖尿病(T2DM)患者体内的循环内皮祖细胞数量较少,这表明EPCs与T2DM相关血管病变之间存在联系。本研究旨在评估NGT、糖耐量受损(IGT)或T2DM的老年人进行急性次最大运动后EPC的数量及动员情况。我们检验了这样一个假设:与NGT相比,IGT患者的EPC动员能力较低,而T2DM老年患者的EPC动员能力则进一步降低。45名年龄在50 - 75岁之间的男性和女性,其中NGT者18例,IGT者10例,T2DM者17例,对其进行了特征描述,并在次最大有氧运动测试前后采集血样,通过流式细胞术对血管内皮生长因子受体2 +(VEGFR2 +)细胞、CD34 +造血祖细胞以及CD34 + / VEGFR2 + EPCs进行计数。与NGT组相比,IGT组和T2DM组的基础EPC数量分别降低了65%和61%(P < 0.05)。NGT组急性运动后EPC数量增加了23%(P < 0.01),而IGT组和T2DM组则无变化。运动前后,VEGFR2 +细胞数量在NGT、IGT和T2DM组中呈逐步降低趋势(P < 0.05)。与NGT组相比,IGT组的基础CD34 +细胞数量较低(P < 0.05),但任何一组运动后该细胞数量均无变化。这些发现提示IGT和T2DM患者存在CD34 + / VEGFR2 + EPC动员缺陷,这可能在与胰岛素抵抗相关的心血管疾病和毛细血管稀疏中发挥作用。

相似文献

1
Exercise-induced endothelial progenitor cell mobilization is attenuated in impaired glucose tolerance and type 2 diabetes.
J Appl Physiol (1985). 2016 Jul 1;121(1):36-41. doi: 10.1152/japplphysiol.00349.2016. Epub 2016 May 19.
2
Serum IL-6 and sIL-6R in type 2 diabetes contribute to impaired capillary-like network formation.
J Appl Physiol (1985). 2019 Aug 1;127(2):385-392. doi: 10.1152/japplphysiol.00002.2019. Epub 2019 Jun 20.
3
Glucose Homeostatic Law: Insulin Clearance Predicts the Progression of Glucose Intolerance in Humans.
PLoS One. 2015 Dec 1;10(12):e0143880. doi: 10.1371/journal.pone.0143880. eCollection 2015.
4
Tumor necrosis factor alpha and insulin resistance in obese type 2 diabetic patients.
Int J Obes Relat Metab Disord. 2003 Jan;27(1):88-94. doi: 10.1038/sj.ijo.0802187.
6
Relationship between serum betatrophin levels and the first-phase of glucose-stimulated insulin secretion.
Obes Res Clin Pract. 2018 Jan-Feb;12(Suppl 2):9-15. doi: 10.1016/j.orcp.2016.08.004. Epub 2016 Aug 21.
7
Elevated 1-h post-load plasma glucose levels in subjects with normal glucose tolerance are associated with a pro-atherogenic lipid profile.
Atherosclerosis. 2017 Jan;256:15-20. doi: 10.1016/j.atherosclerosis.2016.11.020. Epub 2016 Nov 17.
9
Assessing progression to impaired glucose tolerance and type 2 diabetes mellitus.
Eur J Clin Invest. 2006 Nov;36(11):796-802. doi: 10.1111/j.1365-2362.2006.01728.x.

引用本文的文献

2
Circulating endothelial progenitor cells and inflammatory markers in type 1 diabetes after an acute session of aerobic exercise.
Arch Endocrinol Metab. 2024 Nov 6;68(Spec Issue):e230499. doi: 10.20945/2359-4292-2023-0499. eCollection 2024.
5
Roles of physical exercise-induced MiR-126 in cardiovascular health of type 2 diabetes.
Diabetol Metab Syndr. 2022 Nov 14;14(1):169. doi: 10.1186/s13098-022-00942-6.
6
The impact of different forms of exercise on circulating endothelial progenitor cells in cardiovascular and metabolic disease.
Eur J Appl Physiol. 2022 Apr;122(4):815-860. doi: 10.1007/s00421-021-04876-1. Epub 2022 Jan 12.
9
The effects of moderate and high-intensity exercise on circulating markers of endothelial integrity and activation in young, healthy men.
J Appl Physiol (1985). 2019 Nov 1;127(5):1245-1256. doi: 10.1152/japplphysiol.00477.2019. Epub 2019 Sep 5.
10
Exercise and Cardiovascular Progenitor Cells.
Compr Physiol. 2019 Mar 14;9(2):767-797. doi: 10.1002/cphy.c180030.

本文引用的文献

4
Impaired endothelial progenitor cell mobilization and dysfunctional bone marrow stroma in diabetes mellitus.
PLoS One. 2013;8(3):e60357. doi: 10.1371/journal.pone.0060357. Epub 2013 Mar 28.
6
Critical reevaluation of endothelial progenitor cell phenotypes for therapeutic and diagnostic use.
Circ Res. 2012 Feb 17;110(4):624-37. doi: 10.1161/CIRCRESAHA.111.243386.
7
Strategies for enhancing progenitor cell mobilization and function in diabetes.
Curr Vasc Pharmacol. 2012 May;10(3):310-21. doi: 10.2174/157016112799959387.
8
Diagnosis and classification of diabetes mellitus.
Diabetes Care. 2012 Jan;35 Suppl 1(Suppl 1):S64-71. doi: 10.2337/dc12-s064.
9
Diabetes impairs hematopoietic stem cell mobilization by altering niche function.
Sci Transl Med. 2011 Oct 12;3(104):104ra101. doi: 10.1126/scitranslmed.3002191.
10
Endothelial dysfunction in diabetes: the role of reparatory mechanisms.
Diabetes Care. 2011 May;34 Suppl 2(Suppl 2):S285-90. doi: 10.2337/dc11-s239.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验