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高血压患者新发糖尿病与亚临床炎症因子的相关性及机制 被引量:4

Relevance and mechanism of sub-clinical inflammatory factor and new-onset diabetes in patients with primary hypertension
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摘要 目的探讨原发性高血压(高血压)患者新发糖尿病与亚临床炎症的相关性及机制。方法筛选伴腹型肥胖的高血压患者60例设为A组,同期观察健康体检者60名设为正常对照组(B组)。对两组人群同时随访观察,为期3年。如伴腹型肥胖高血压患者新发糖尿病设为C组,对3组人群进行空腹血糖、空腹胰岛素水平、餐后2 h血糖、超敏C反应蛋白、纤维蛋白原、肿瘤坏死因子-α以及单核细胞过氧化物酶体增生物激活受体(peroxisome proliferator-activated receptor,PPARγ)的表达水平进行测定,观察炎性标志物水平与新发糖尿病的关系,及其对PPARγ表达的影响。结果经随访观察3年,A组新发糖尿病22例,发病率36.7%;B组出现高血压并同时伴有腹型肥胖者8例,出现伴腹型肥胖高血压新发糖尿病者1例。高血压新发糖尿病组患者空腹血糖、餐后2 h血糖、空腹胰岛素水平、超敏C反应蛋白[(4.23±2.2)mg/L vs.(3.62±1.18)mg/L,P<0.01;(4.23±2.2)mg/L vs.(1.74±0.77)mg/L,P<0.01]、纤维蛋白原[(4.38±0.77)g/L vs.(2.87±0.62)g/L,P<0.01;(4.38±0.77)g/L vs.(2.25±0.58)g/L,P<0.01]、肿瘤坏死因子-α[(10.2±4.3)ng/L vs.(4.47±1.31)ng/L,P<0.01;(10.2±4.3)ng/L vs.(2.68±0.78)ng/L,P<0.01]均显著高于健康对照组及伴腹型肥胖高血压组患者,PPARγ均低于两组[5.57±0.73 vs.8.52±0.88,P<0.01;5.57±0.73 vs.10.44±1.87,P<0.01],差异有统计学意义。结论慢性炎症状态可能是高血压患者易发2型糖尿病的重要危险因素,PPARγ表达降低可能是慢性炎症状态导致新发糖尿病发生的机制之一。 Objectives To explore the relevance and mechanism of sub-clinical inflammatory factor and new-onset diabetes in patients with primary hypertension. Methods Sixty hypertensive patients with abdominal obesity (group A) and 60 healthy cases (group B) were followed-up for 3 years. If the new-onset diabetes were found in group A, they would be attributed to group C. Content of fasting blood glucose, fasting insulin levels, postprandial 2 h blood glucose, high sensitivity creactive protein (CRP), fibrinogen (FIB), tumor necrosis factor alpha (TNF-ct) and peroxisome proliferator- activated receptor (PPAR) gamma expression level were compared among these three groups. Results After followed up for 3 years, 22 cases with new-onset diabetes were found in group A. Eight hypertensive patients with abdominal obesity in group B were also found, and only one new-onset diabetes was found. Content of fasting blood glucose, fasting insulin levels, postprandial 2 h blood glucose, CRP[(4.23±2.2) mg/L vs. (3.62±l.18)mg/L, P〈0.01 ; (4.23±2.2) mg/L vs. (1.74±0.77) rag/L, P〈0.01], FIB[(4.38±0.77) g/L vs. (2.87±0.62) g/L, P〈0.01 ; (4.38±0.77) g/L vs. (2.25±0.58) g/L, P〈0.01] and TNF-a[(10.2±4.3) ng/Lvs. (4.47±1.31) ng/L, P〈0.01; (10.2±4.3) ng/L vs. (2.68±0.78) ng/L, P〈0.01 ] in group C were significantly higher than those in group B and group A, but PPAR gamma expression level in group C was less than that in group B and group A [5.57±0.73 vs.8.52±0.88, P〈0.01;5.57±0.73 vs. 10.44±1.87, P〈0.011, which showed significant difference. Conclusions Chronic inflammation state may be the important risk factors of hypertension patients with type 2 diabetes. Decreasing express of PPAR gamma may be one of the mechanism of chronic inflammation to induce new-onset diabetes.
出处 《岭南心血管病杂志》 2011年第4期281-284,共4页 South China Journal of Cardiovascular Diseases
关键词 高血压 糖尿病 超敏C反应蛋白 纤维蛋白原 肿瘤坏死因子-Α 过氧化物酶体增生物激活受体 hypertension diabetes high sensitivity C-reactive protein fibrinogen tumor necrosis factor alpha peroxisome proliferator-aetivated receptor
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