Department of Clinical and Chemical Pathology, Medical Research Division, National Research Center, Cairo, Egypt.
J Diabetes Complications. 2019 Nov;33(11):107421. doi: 10.1016/j.jdiacomp.2019.107421. Epub 2019 Aug 22.
Although previous data have suggested ANGPTL2 and ANGPTL8 (betatrophin) to be related to atherosclerosis in humans, little is known whether this applies in patients with type 2 diabetes (T2D). In this work, we investigate association of serum ANGPTL2 and betatrophin with the risk of cardiovascular diseases (CVD) in T2D patients.
We measured serum levels of ANGPTL2 and betatrophin in 150 T2D patients with and without CVD and in 100 control subjects.
Serum ANGPTL2 was significantly higher in T2D patients than in controls (p < 0.0001), and in T2D + CVD patients than T2D only patients (p = 0.0002). Serum betatrophin was lower in T2D patients than in controls but with no statistical significance (p = 0.07). Elevated serum ANGPTL2 associated with 2.83-fold increased risk of T2D and with 1.18-fold elevated risk of CVD among T2D patients with positive correlations with markers of hyperglycemia, insulin resistance and atherogenic lipid profile. ROC curve indicated ANGPTL2 as risk biomarker for T2D and CVD with sensitivity of 92.2% and 86%; and specificity of 86.7% and 58%; respectively.
We indicate for the first time serum ANGPTL2 as an independent risk biomarker for CVD in T2D patients. Future studies are needed to reveal its role in disease pathogenesis.
尽管先前的数据表明 ANGPTL2 和 ANGPTL8(betatrophin)与人类的动脉粥样硬化有关,但尚不清楚这是否适用于 2 型糖尿病(T2D)患者。在这项工作中,我们研究了血清 ANGPTL2 和 betatrophin 与 T2D 患者发生心血管疾病(CVD)风险的相关性。
我们测量了 150 例有和无 CVD 的 T2D 患者以及 100 例对照者的血清 ANGPTL2 和 betatrophin 水平。
T2D 患者的血清 ANGPTL2 水平明显高于对照组(p<0.0001),且 T2D+CVD 患者高于 T2D 仅患者(p=0.0002)。T2D 患者的血清 betatrophin 水平低于对照组,但无统计学意义(p=0.07)。升高的血清 ANGPTL2 与 T2D 的风险增加 2.83 倍相关,与 T2D 患者的 CVD 风险增加 1.18 倍相关,且与高血糖、胰岛素抵抗和致动脉粥样硬化脂质谱的标志物呈正相关。ROC 曲线表明 ANGPTL2 是 T2D 和 CVD 的风险生物标志物,其敏感性分别为 92.2%和 86%;特异性分别为 86.7%和 58%。
我们首次表明血清 ANGPTL2 是 T2D 患者 CVD 的独立风险生物标志物。需要进一步的研究来揭示其在疾病发病机制中的作用。