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Decreased Insulin Sensitivity and Impaired Fibrinolytic Activity in Type 2 Diabetes Patients and Nondiabetics with Ischemic Stroke

机译:2型糖尿病和非糖尿病性缺血性卒中患者胰岛素敏感性降低和纤溶活性受损

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摘要

We analyzed (a) insulin sensitivity (IS), (b) plasma insulin (PI), and (c) plasminogen activator inhibitor-1 (PAI-1) in type 2 diabetes (T2D) patients with (group A) and without (group B) atherothrombotic ischemic stroke (ATIS), nondiabetics with ATIS (group C), and healthy controls (group D). IS was determined by minimal model (Si). Si was lower in A versus B (1.18 ± 0.67 versus 2.82 ± 0.61 min−1/mU/L × 104; P < 0.001) and in C versus D (3.18 ± 0.93 versus 6.13 ± 1.69 min−1/mU/L × 104; P < 0.001). PI and PAI-1 were higher in A versus B (PI: 19.61 ± 4.08 versus 14.91 ± 1.66 mU/L; P < 0.001, PAI-1: 7.75 ± 1.04 versus 4.57 ± 0.72 mU/L; P < 0.001) and in C versus D (PI: 15.14 ± 2.20 versus 7.58 ± 2.05 mU/L; P < 0.001, PAI-1: 4.78 ± 0.98 versus 3.49 ± 1.04 mU/L; P < 0.001). Si correlated with PAI-1 in T2D patients and nondiabetics, albeit stronger in T2D. Binary logistic regression identified insulin, PAI-1, and Si as independent predictors for ATIS in T2D patients and nondiabetics. The results imply that insulin resistance and fasting hyperinsulinemia might exert their atherogenic impact through the impaired fibrinolysis.
机译:我们分析了(a)组和不具有(a)组的2型糖尿病(T2D)患者的(a)胰岛素敏感性(IS),(b)血浆胰岛素(PI)和(c)纤溶酶原激活物抑制剂1(PAI-1)。 B组)动脉粥样硬化血栓形成性缺血性中风(ATIS),非糖尿病伴ATIS(C组)和健康对照组(D组)。 IS由最小模型(Si)确定。 A相对于B的Si较低(1.18±0.67相对2.82±0.61 min-1 / mU / L×104; P <0.001),而C相对于D(3.18±0.93相对6.13±1.69 min-1 / mU / L× 104; P <0.001)。 PI和PAI-1在A组中高于B组(PI:19.61±4.08对14.91±1.66µmU / L; P <0.001,PAI-1:7.75±1.04对4.57±0.72µmU / L; P <0.001) C vs D(PI:15.14±2.20 vs 7.58±2.05µmU / L; P <0.001,PAI-1:4.78±0.98 vs 3.49±1.04µmU / L; P <0.001)。 Si在T2D患者和非糖尿病患者中与PAI-1相关,尽管在T2D中更强。二进制逻辑回归分析确定胰岛素,PAI-1和Si是T2D患者和非糖尿病患者ATIS的独立预测因子。结果暗示胰岛素抵抗和空腹高胰岛素血症可能通过受损的纤维蛋白溶解发挥其动脉粥样硬化作用。

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