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加纳一家三级医院糖尿病患者体内的循环血管生成因子

Circulating angiogenic factors in diabetes patients in a tertiary hospital in Ghana.

作者信息

Yeboah Kwame, Kyei-Baafour Eric, Antwi Daniel A, Asare-Anane Henry, Gyan Ben, Amoah Albert G B

机构信息

Department of Physiology, School of Biomedical and Allied Health Sciences, University of Ghana, P O Box KB143, Korle-Bu, Accra, Ghana.

Department of Immunology, Noguchi Memorial Institute of Medical Research, University of Ghana, Accra, Ghana.

出版信息

J Diabetes Metab Disord. 2016 Oct 10;15:44. doi: 10.1186/s40200-016-0267-1. eCollection 2016.

DOI:10.1186/s40200-016-0267-1
PMID:27777900
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5057505/
Abstract

BACKGROUND

Impaired angiogenesis is amongst the underlining mechanisms of organ damage in diabetes and hypertensive patients. In diabetes and hypertensive patients without proteinuria and overt CVDs, we studied the levels of angiogenic growth factors, angiopoietin (Ang)-1, Ang-2 and vascular endothelial growth factor (VEGF), and the relationship between these angiogenic growth factors and renal function, measured as estimated glomerular filtration rate (eGFR).

METHOD

In a case control design, 107 type 2 diabetes (T2DM) patients and 93 non-diabetes controls were recruited into the study. Levels of plasma glucose, lipids, creatinine and angiogenic growth factors; Ang-1, Ang-2 and VEGF measured from fasting blood samples. Estimated glomerular filtration rate (eGFR) was computed using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) algorithm and eGFR < 60 ml/min/1.73 m was considered to be low. Multivariable logistic regression was used to assess the odds of change in angiogenic growth factors among patients with diabetes and hypertension, and patients with low eGFR, compared to those without these conditions.

RESULTS

In a total of 200 participants with 49 % females and mean age of 54.1 ± 10.2 years, 22.7 % of T2DM patients and 13.3 % of non-diabetes participant had low eGFR. The levels of Ang-1 and Ang-2 were highest in hypertensive T2DM patients, followed by patients with either T2DM or hypertension alone, with the controls having the lowest levels. The odds of change in circulating Ang-2 levels increased in patients with both diabetes and hypertension [11.76 (7.97-16.63),  < 0.01] compared to patients with either diabetes [5.45 (3.31-9.71),  = 0.02] or hypertension [5.45 (3.31-9.71),  = 0.02] alone. Compared to those with normal eGFR, the odds of change in serum Ang-2 levels were increased in patients with low eGFR in both the crude [1.26 (1.08-2.110),  = 0.023] and adjusted [1.14 (1.03-2.34),  = 0.043] regression models.

CONCLUSION

In our study population, having diabetes and hypertension increased the levels of Ang-1 and Ang-2. Also, low eGFR status was associated with increased levels of Ang-2 after adjustment for other risk factors.

摘要

背景

血管生成受损是糖尿病和高血压患者器官损伤的潜在机制之一。在无蛋白尿和明显心血管疾病的糖尿病和高血压患者中,我们研究了血管生成生长因子、血管生成素(Ang)-1、Ang-2和血管内皮生长因子(VEGF)的水平,以及这些血管生成生长因子与以估计肾小球滤过率(eGFR)衡量的肾功能之间的关系。

方法

采用病例对照设计,招募了107例2型糖尿病(T2DM)患者和93例非糖尿病对照者进入研究。从空腹血样中检测血浆葡萄糖、脂质、肌酐和血管生成生长因子;Ang-1、Ang-2和VEGF的水平。使用慢性肾脏病流行病学协作组(CKD-EPI)算法计算估计肾小球滤过率(eGFR),eGFR<60 ml/min/1.73 m²被认为较低。采用多变量逻辑回归评估糖尿病和高血压患者以及eGFR较低的患者与无这些情况的患者相比,血管生成生长因子变化的几率。

结果

在总共200名参与者中,女性占49%,平均年龄为54.1±10.2岁,22.7%的T2DM患者和13.3%的非糖尿病参与者eGFR较低。Ang-1和Ang-2水平在高血压T2DM患者中最高,其次是仅患有T2DM或高血压的患者,对照组水平最低。与仅患有糖尿病[5.45(3.31-9.71),P=0.02]或高血压[5.45(3.31-9.71),P=0.02]的患者相比,糖尿病和高血压患者循环Ang-2水平变化的几率增加[11.76(7.97-16.63),P<0.01]。与eGFR正常的患者相比,在粗回归模型[1.26(1.08-2.110),P=0.023]和调整回归模型[1.14(1.03-2.34),P=0.043]中,eGFR较低的患者血清Ang-2水平变化的几率均增加。

结论

在我们的研究人群中,患有糖尿病和高血压会增加Ang-1和Ang-2的水平。此外,在调整其他危险因素后,低eGFR状态与Ang-2水平升高有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/bcb3065c9118/40200_2016_267_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/d1862de0b85b/40200_2016_267_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/6dee2e609f6c/40200_2016_267_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/bcb3065c9118/40200_2016_267_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/d1862de0b85b/40200_2016_267_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/6dee2e609f6c/40200_2016_267_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2607/5057505/bcb3065c9118/40200_2016_267_Fig3_HTML.jpg

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