Alicia J Jenkins, Jeffrey D McBride, Andrzej S Januszewski, Connie S Karschimkus, Bin Zhang, David N O'Neal, Craig L Nelson, Jasmine S Chung, C Alex Harper, Timothy J Lyons, Jian-Xing Ma
{"title":"伴有血管并发症的1型糖尿病患者血清卡利司他汀水平升高","authors":"Alicia J Jenkins, Jeffrey D McBride, Andrzej S Januszewski, Connie S Karschimkus, Bin Zhang, David N O'Neal, Craig L Nelson, Jasmine S Chung, C Alex Harper, Timothy J Lyons, Jian-Xing Ma","doi":"10.1186/2040-2384-2-19","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Kallistatin, a serpin widely produced throughout the body, has vasodilatory, anti-angiogenic, anti-oxidant, and anti-inflammatory effects. Effects of diabetes and its vascular complications on serum kallistatin levels are unknown.</p><p><strong>Methods: </strong>Serum kallistatin was quantified by ELISA in a cross-sectional study of 116 Type 1 diabetic patients (including 50 with and 66 without complications) and 29 non-diabetic controls, and related to clinical status and measures of oxidative stress and inflammation.</p><p><strong>Results: </strong>Kallistatin levels (mean(SD)) were increased in diabetic vs. control subjects (12.6(4.2) vs. 10.3(2.8) μg/ml, p = 0.007), and differed between diabetic patients with complications (13.4(4.9) μg/ml), complication-free patients (12.1(3.7) μg/ml), and controls; ANOVA, p = 0.007. Levels were higher in diabetic patients with complications vs. controls, p = 0.01, but did not differ between complication-free diabetic patients and controls, p > 0.05. On univariate analyses, in diabetes, kallistatin correlated with renal dysfunction (cystatin C, r = 0.28, p = 0.004; urinary albumin/creatinine, r = 0.34, p = 0.001; serum creatinine, r = 0.23, p = 0.01; serum urea, r = 0.33, p = 0.001; GFR, r = -0.25, p = 0.009), total cholesterol (r = 0.28, p = 0.004); LDL-cholesterol (r = 0.21, p = 0.03); gamma-glutamyltransferase (GGT) (r = 0.27, p = 0.04), and small artery elasticity, r = -0.23, p = 0.02, but not with HbA1c, other lipids, oxidative stress or inflammation. In diabetes, geometric mean (95%CI) kallistatin levels adjusted for covariates, including renal dysfunction, were higher in those with vs. without hypertension (13.6 (12.3-14.9) vs. 11.8 (10.5-13.0) μg/ml, p = 0.03). Statistically independent determinants of kallistatin levels in diabetes were age, serum urea, total cholesterol, SAE and GGT, adjusted r2 = 0.24, p < 0.00001.</p><p><strong>Conclusions: </strong>Serum kallistatin levels are increased in Type 1 diabetic patients with microvascular complications and with hypertension, and correlate with renal and vascular dysfunction.</p>","PeriodicalId":88540,"journal":{"name":"Journal of angiogenesis research","volume":"2 ","pages":"19"},"PeriodicalIF":0.0000,"publicationDate":"2010-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-2384-2-19","citationCount":"37","resultStr":"{\"title\":\"Increased serum kallistatin levels in type 1 diabetes patients with vascular complications.\",\"authors\":\"Alicia J Jenkins, Jeffrey D McBride, Andrzej S Januszewski, Connie S Karschimkus, Bin Zhang, David N O'Neal, Craig L Nelson, Jasmine S Chung, C Alex Harper, Timothy J Lyons, Jian-Xing Ma\",\"doi\":\"10.1186/2040-2384-2-19\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Kallistatin, a serpin widely produced throughout the body, has vasodilatory, anti-angiogenic, anti-oxidant, and anti-inflammatory effects. Effects of diabetes and its vascular complications on serum kallistatin levels are unknown.</p><p><strong>Methods: </strong>Serum kallistatin was quantified by ELISA in a cross-sectional study of 116 Type 1 diabetic patients (including 50 with and 66 without complications) and 29 non-diabetic controls, and related to clinical status and measures of oxidative stress and inflammation.</p><p><strong>Results: </strong>Kallistatin levels (mean(SD)) were increased in diabetic vs. control subjects (12.6(4.2) vs. 10.3(2.8) μg/ml, p = 0.007), and differed between diabetic patients with complications (13.4(4.9) μg/ml), complication-free patients (12.1(3.7) μg/ml), and controls; ANOVA, p = 0.007. Levels were higher in diabetic patients with complications vs. controls, p = 0.01, but did not differ between complication-free diabetic patients and controls, p > 0.05. On univariate analyses, in diabetes, kallistatin correlated with renal dysfunction (cystatin C, r = 0.28, p = 0.004; urinary albumin/creatinine, r = 0.34, p = 0.001; serum creatinine, r = 0.23, p = 0.01; serum urea, r = 0.33, p = 0.001; GFR, r = -0.25, p = 0.009), total cholesterol (r = 0.28, p = 0.004); LDL-cholesterol (r = 0.21, p = 0.03); gamma-glutamyltransferase (GGT) (r = 0.27, p = 0.04), and small artery elasticity, r = -0.23, p = 0.02, but not with HbA1c, other lipids, oxidative stress or inflammation. In diabetes, geometric mean (95%CI) kallistatin levels adjusted for covariates, including renal dysfunction, were higher in those with vs. without hypertension (13.6 (12.3-14.9) vs. 11.8 (10.5-13.0) μg/ml, p = 0.03). Statistically independent determinants of kallistatin levels in diabetes were age, serum urea, total cholesterol, SAE and GGT, adjusted r2 = 0.24, p < 0.00001.</p><p><strong>Conclusions: </strong>Serum kallistatin levels are increased in Type 1 diabetic patients with microvascular complications and with hypertension, and correlate with renal and vascular dysfunction.</p>\",\"PeriodicalId\":88540,\"journal\":{\"name\":\"Journal of angiogenesis research\",\"volume\":\"2 \",\"pages\":\"19\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2010-09-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1186/2040-2384-2-19\",\"citationCount\":\"37\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of angiogenesis research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/2040-2384-2-19\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of angiogenesis research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/2040-2384-2-19","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 37
摘要
背景:卡利司他汀是一种在全身广泛产生的蛇形蛋白，具有血管扩张、抗血管生成、抗氧化和抗炎作用。糖尿病及其血管并发症对血清卡利司他汀水平的影响尚不清楚。方法:采用ELISA法对116例1型糖尿病患者(合并并发症50例，无并发症66例)和29例非糖尿病对照进行血清卡利司他汀定量分析，并与临床状态、氧化应激和炎症指标进行比较。结果:糖尿病组卡利司他汀水平(SD)高于对照组(12.6(4.2)vs. 10.3(2.8) μg/ml, p = 0.007)，有并发症组(13.4(4.9)μg/ml)、无并发症组(12.1(3.7)μg/ml)和对照组差异显著;方差分析，p = 0.007。有并发症的糖尿病患者血清水平高于对照组，p = 0.01，无并发症的糖尿病患者与对照组无差异，p > 0.05。单因素分析显示，在糖尿病患者中，卡利司他汀与肾功能障碍相关(胱抑素C, r = 0.28, p = 0.004;尿白蛋白/肌酐，r = 0.34, p = 0.001;血清肌酐，r = 0.23, p = 0.01;血清尿素，r = 0.33, p = 0.001;GFR (r = -0.25, p = 0.009)、总胆固醇(r = 0.28, p = 0.004);低密度脂蛋白胆固醇(r = 0.21, p = 0.03);γ -谷氨酰转移酶(GGT) (r = 0.27, p = 0.04)和小动脉弹性(r = -0.23, p = 0.02)，但与糖化血红蛋白、其他脂质、氧化应激或炎症无关。在糖尿病患者中，经包括肾功能在内的协变量调整后的几何平均(95%CI)卡列他汀水平在高血压患者中高于非高血压患者(13.6 (12.3-14.9)vs 11.8 (10.5-13.0) μg/ml, p = 0.03)。糖尿病患者卡利司他汀水平的统计独立决定因素为年龄、血清尿素、总胆固醇、SAE和GGT，校正r2 = 0.24, p < 0.00001。结论:伴有微血管并发症和高血压的1型糖尿病患者血清卡利司他汀水平升高，并与肾脏和血管功能障碍相关。
Increased serum kallistatin levels in type 1 diabetes patients with vascular complications.
Background: Kallistatin, a serpin widely produced throughout the body, has vasodilatory, anti-angiogenic, anti-oxidant, and anti-inflammatory effects. Effects of diabetes and its vascular complications on serum kallistatin levels are unknown.
Methods: Serum kallistatin was quantified by ELISA in a cross-sectional study of 116 Type 1 diabetic patients (including 50 with and 66 without complications) and 29 non-diabetic controls, and related to clinical status and measures of oxidative stress and inflammation.
Results: Kallistatin levels (mean(SD)) were increased in diabetic vs. control subjects (12.6(4.2) vs. 10.3(2.8) μg/ml, p = 0.007), and differed between diabetic patients with complications (13.4(4.9) μg/ml), complication-free patients (12.1(3.7) μg/ml), and controls; ANOVA, p = 0.007. Levels were higher in diabetic patients with complications vs. controls, p = 0.01, but did not differ between complication-free diabetic patients and controls, p > 0.05. On univariate analyses, in diabetes, kallistatin correlated with renal dysfunction (cystatin C, r = 0.28, p = 0.004; urinary albumin/creatinine, r = 0.34, p = 0.001; serum creatinine, r = 0.23, p = 0.01; serum urea, r = 0.33, p = 0.001; GFR, r = -0.25, p = 0.009), total cholesterol (r = 0.28, p = 0.004); LDL-cholesterol (r = 0.21, p = 0.03); gamma-glutamyltransferase (GGT) (r = 0.27, p = 0.04), and small artery elasticity, r = -0.23, p = 0.02, but not with HbA1c, other lipids, oxidative stress or inflammation. In diabetes, geometric mean (95%CI) kallistatin levels adjusted for covariates, including renal dysfunction, were higher in those with vs. without hypertension (13.6 (12.3-14.9) vs. 11.8 (10.5-13.0) μg/ml, p = 0.03). Statistically independent determinants of kallistatin levels in diabetes were age, serum urea, total cholesterol, SAE and GGT, adjusted r2 = 0.24, p < 0.00001.
Conclusions: Serum kallistatin levels are increased in Type 1 diabetic patients with microvascular complications and with hypertension, and correlate with renal and vascular dysfunction.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
