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本文引用的文献

1
Total serum bilirubin does not affect vascular reactivity in patients with diabetes.总血清胆红素不影响糖尿病患者的血管反应性。
Vasc Med. 2009 May;14(2):129-36. doi: 10.1177/1358863X08098273.
2
Diagnosis and classification of diabetes mellitus.糖尿病的诊断与分类
Diabetes Care. 2009 Jan;32 Suppl 1(Suppl 1):S62-7. doi: 10.2337/dc09-S062.
3
The role of vascular endothelial growth factor in wound healing.血管内皮生长因子在伤口愈合中的作用。
J Surg Res. 2009 May 15;153(2):347-58. doi: 10.1016/j.jss.2008.04.023. Epub 2008 May 12.
4
General and abdominal adiposity and risk of death in Europe.欧洲的总体及腹部肥胖与死亡风险
N Engl J Med. 2008 Nov 13;359(20):2105-20. doi: 10.1056/NEJMoa0801891.
5
Clinical analysis of the soft tissue integration of non-submerged (ITI) and submerged (3i) implants: a prospective-controlled cohort study.非潜入式(ITI)和潜入式(3i)种植体软组织整合的临床分析:一项前瞻性对照队列研究。
Clin Oral Implants Res. 2008 Oct;19(10):991-6. doi: 10.1111/j.1600-0501.2007.01345.x.
6
Impaired endothelium-dependent vasodilation in overweight and obese adult humans is not limited to muscarinic receptor agonists.超重和肥胖成年人中内皮依赖性血管舒张功能受损并不局限于毒蕈碱受体激动剂。
Am J Physiol Heart Circ Physiol. 2008 Apr;294(4):H1685-92. doi: 10.1152/ajpheart.01281.2007. Epub 2008 Feb 15.
7
Relation of cumulative weight burden to vascular endothelial dysfunction in obesity.肥胖中累积体重负担与血管内皮功能障碍的关系。
Am J Cardiol. 2008 Jan 1;101(1):98-101. doi: 10.1016/j.amjcard.2007.07.055.
8
Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice.骨桥蛋白介导肥胖诱导的小鼠脂肪组织巨噬细胞浸润和胰岛素抵抗。
J Clin Invest. 2007 Oct;117(10):2877-88. doi: 10.1172/JCI31986.
9
Angiogenesis modulates adipogenesis and obesity.血管生成调节脂肪生成和肥胖。
J Clin Invest. 2007 Sep;117(9):2362-8. doi: 10.1172/JCI32239.
10
Plasma osteopontin levels and expression in adipose tissue are increased in obesity.肥胖时血浆骨桥蛋白水平及脂肪组织中的表达会升高。
J Clin Endocrinol Metab. 2007 Sep;92(9):3719-27. doi: 10.1210/jc.2007-0349. Epub 2007 Jun 26.

糖尿病和肥胖对血管反应性、炎症细胞因子和生长因子的影响。

Effects of diabetes and obesity on vascular reactivity, inflammatory cytokines, and growth factors.

机构信息

Microcirculation Laboratory, Joslin-Beth Israel Deaconess Foot Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Obesity (Silver Spring). 2011 Apr;19(4):729-35. doi: 10.1038/oby.2010.193. Epub 2010 Sep 9.

DOI:10.1038/oby.2010.193
PMID:20829804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3676733/
Abstract

We examined the influences of obesity and diabetes on endothelium-dependent and -independent vasodilation, inflammatory cytokines, and growth factors. We included 258 subjects, age 21-80 years in four groups matched for age and gender: 40 healthy nonobese (BMI <30 kg·m(-2)) nondiabetic subjects, 76 nonobese diabetic patients, 37 obese (BMI >30) nondiabetic subjects, and 105 obese (BMI >30) diabetic patients. The flow-mediated dilation (FMD, endothelium-dependent) and nitroglycerin-induced dilation (NID, endothelium-independent) in the brachial artery, the vascular reactivity at the forearm skin and serum growth factors and inflammatory cytokines were measured. FMD was reduced in the nonobese diabetic patients, obese nondiabetic controls, and obese diabetic patients (P < 0.0001). NID was different among all four groups, being highest in the obese nondiabetic subjects and lowest in the obese diabetic patients (P < 0.0001). The resting skin forearm blood flow was reduced in the obese nondiabetic subjects (P < 0.01). Vascular endothelial growth factor (VEGF) was higher in the obese nondiabetic subjects (P < 0.05), tumor necrosis factor-α was higher in the obese diabetic patients (P < 0.0001) and C-reactive protein was higher in both the obese nondiabetic and diabetic subjects (P < 0.0001). Soluble intercellular adhesion molecule-1 was elevated in the two diabetic groups and the obese nondiabetic subjects (P < 0.05). We conclude that diabetes and obesity affect equally the endothelial cell function but the smooth muscle cell function is affected only by diabetes. In addition, the above findings may be related to differences that were observed in the growth factors and inflammatory cytokines.

摘要

我们研究了肥胖和糖尿病对内皮依赖性和非依赖性血管舒张、炎症细胞因子和生长因子的影响。我们纳入了 258 名年龄在 21-80 岁的受试者,他们按年龄和性别分为四组:40 名健康非肥胖(BMI<30kg·m(-2))非糖尿病患者、76 名非肥胖糖尿病患者、37 名肥胖(BMI>30)非糖尿病患者和 105 名肥胖(BMI>30)糖尿病患者。肱动脉的血流介导的扩张(FMD,内皮依赖性)和硝酸甘油诱导的扩张(NID,内皮非依赖性)、前臂皮肤的血管反应性以及血清生长因子和炎症细胞因子均进行了测量。非肥胖糖尿病患者、肥胖非糖尿病对照组和肥胖糖尿病患者的 FMD 均降低(P<0.0001)。四组之间的 NID 不同,肥胖非糖尿病患者的 NID 最高,肥胖糖尿病患者的 NID 最低(P<0.0001)。肥胖非糖尿病患者的静息前臂皮肤血流减少(P<0.01)。肥胖非糖尿病患者的血管内皮生长因子(VEGF)升高(P<0.05),肥胖糖尿病患者的肿瘤坏死因子-α升高(P<0.0001),肥胖非糖尿病和糖尿病患者的 C 反应蛋白升高(P<0.0001)。两种糖尿病组和肥胖非糖尿病组的可溶性细胞间黏附分子-1 升高(P<0.05)。我们得出结论,糖尿病和肥胖对内皮细胞功能的影响相同,但平滑肌细胞功能仅受糖尿病影响。此外,上述发现可能与生长因子和炎症细胞因子的差异有关。