Krisai Philipp, Leib Stefanie, Aeschbacher Stefanie, Kofler Thomas, Assadian Mustafa, Maseli Anna, Todd John, Estis Joel, Risch Martin, Risch Lorenz, Conen David
Department of Medicine, University Hospital Basel, Petersgraben 4, 4031 Basel, Switzerland; Cardiovascular Research Institute Basel, University Hospital Basel, Switzerland.
Cardiovascular Research Institute Basel, University Hospital Basel, Switzerland.
Eur J Intern Med. 2016 Jul;32:31-7. doi: 10.1016/j.ejim.2016.03.017. Epub 2016 Apr 21.
Several biomarkers within the iron metabolism pathway have been related to the occurrence of diabetes mellitus, but underlying mechanisms are unknown. The aim of our study was to investigate the differential relationships of iron metabolism with a broad range of diabetes markers in young and healthy adults.
2160 participants aged 25 to 41years were enrolled in a population-based study. Established cardiovascular disease, diabetes or a body mass index >35kg/m(2) were exclusion criteria. Multivariable linear regression models were built to assess the associations of ferritin and transferrin saturation (TSAT) with blood levels of glucagon-like peptide-1 (GLP-1), insulin, homeostatic model assessment-insulin resistance (HOMA-IR), fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c).
Median (interquartile range) age was 37 (31, 40) years. In multivariable linear regression analyses, β-coefficients (95% confidence intervals) per 1-SD increase in ferritin were 0.04 (0.02; 0.07, p=0.0008) for GLP-1, 0.06 (0.04; 0.08, p<0.0001) for insulin, 0.07 (0.04; 0.09, p<0.0001) for HOMA-IR, 0.004 (-0.00; 0.01, p=0.07) for FPG and -0.003 (-0.01; -0.00, p=0.07) for HbA1c. β-coefficients (95% CI) per 1-SD increase in TSAT were -0.07 (-0.09; -0.05, p<0.0001) for GLP-1, -0.06 (-0.08; -0.04, p<0.0001) for insulin, -0.07(-0.09; -0.05, p<0.0001) for HOMA-IR, -0.01 (-0.01; -0.00, p<0.0001) for FPG and -0.01 (-0.01; -0.00, p=0.0004) for HbA1c.
Markers of insulin resistance are strongly related with markers of iron metabolism in healthy subjects. These relationships were inconsistent and weaker for short-term and long-term glucose levels. These results may provide insights in the relationships between iron metabolism and diabetes occurrence.
铁代谢途径中的几种生物标志物与糖尿病的发生有关,但其潜在机制尚不清楚。我们研究的目的是调查铁代谢与年轻健康成年人中广泛的糖尿病标志物之间的差异关系。
2160名年龄在25至41岁的参与者被纳入一项基于人群的研究。排除标准为已确诊的心血管疾病、糖尿病或体重指数>35kg/m²。建立多变量线性回归模型以评估铁蛋白和转铁蛋白饱和度(TSAT)与胰高血糖素样肽-1(GLP-1)、胰岛素、稳态模型评估胰岛素抵抗(HOMA-IR)、空腹血糖(FPG)和糖化血红蛋白(HbA1c)血液水平之间的关联。
年龄中位数(四分位间距)为37(31,40)岁。在多变量线性回归分析中,铁蛋白每增加1个标准差,GLP-1的β系数(95%置信区间)为0.04(0.02;0.07,p=0.0008),胰岛素为0.06(0.04;0.08,p<0.0001),HOMA-IR为0.07(0.04;0.09,p<0.0001),FPG为0.004(-0.00;0.01,p=0.07),HbA1c为-0.003(-0.01;-0.00,p=0.07)。TSAT每增加1个标准差,GLP-1的β系数(95%CI)为-0.07(-0.09;-0.05,p<0.0001),胰岛素为-0.06(-0.08;-0.04,p<0.0001),HOMA-IR为-0.07(-0.09;-0.05,p<0.0001),FPG为-0.01(-0.01;-0.00,p<0.0001),HbA1c为-0.01(-0.01;-0.00,p=0.0004)。
在健康受试者中,胰岛素抵抗标志物与铁代谢标志物密切相关。对于短期和长期血糖水平,这些关系不一致且较弱。这些结果可能为铁代谢与糖尿病发生之间的关系提供见解。