Yanai Hidekatsu, Katsuyama Hisayuki, Hakoshima Mariko
Department of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine Kohnodai Hospital, Chiba, Japan.
Cardiol Res. 2021 Dec;12(6):358-362. doi: 10.14740/cr1333. Epub 2021 Nov 29.
Dyslipidemia is one of the major risk factors for cardiovascular disease (CVD), along with hypertension, diabetes, smoking and obesity. Approximately 70% of CVD risk remains even after treatment of elevated low-density lipoprotein-cholesterol (LDL-C) by statins. High triglyceride (TG) and low high-density lipoprotein-cholesterol (HDL-C) level are potential therapeutic targets to prevent CVD. Fibrates were associated with a greater reduction in TG, and a greater increase in HDL-C. Fibrates activate specific transcription factors belonging to the nuclear hormone receptor superfamily, termed peroxisome proliferator-activated receptors (PPARs). Fibrates improve atherogenic dyslipidemia by mediating PPARα. Pemafibrate is a novel member of the selective PPARα modulator (SPPARMα) family that was designed to have a higher PPARα agonistic activity and selectivity than previous fibrates. Here, we aimed to study the influences of the switching from fenofibrate to pemafibrate on metabolic parameters in type 2 diabetic patients.
We retrospectively picked up type 2 diabetic patients who had undergone the switching from fenofibrate to pemafibrate, and compared metabolic parameters before the switching with the data at 3, 6 and 12 months after the switching.
We found 15 patients with type 2 diabetes. Serum alanine aminotransferase significantly decreased at 6 months after the switching as compared with baseline. The estimated glomerular filtration rate (eGFR) significantly increased at 3, 6 and 12 months after the switching from fenofibrate to pemafibrate as compared with baseline. Serum uric acid (UA) levels significantly increased at 3 and 6 months after the switching as compared with baseline. We did not observe changes in other metabolic parameters after the switching.
We observed a significant increase of eGFR and serum UA after the switching from fenofibrate to pemafibrate in type 2 diabetic patients. Recent evidences suggest that the improvement of eGFR is beneficially associated with the development of CVD in type 2 diabetic patients. Considering the impact on eGFR, pemafibrate may effectively reduce CVD as compared with fenofibrate.
血脂异常是心血管疾病（CVD）的主要危险因素之一，与高血压、糖尿病、吸烟和肥胖并列。即使通过他汀类药物治疗升高的低密度脂蛋白胆固醇（LDL-C）后，仍有大约70%的CVD风险存在。高甘油三酯（TG）和低高密度脂蛋白胆固醇（HDL-C）水平是预防CVD的潜在治疗靶点。贝特类药物与更大程度地降低TG以及更大程度地升高HDL-C相关。贝特类药物激活属于核激素受体超家族的特定转录因子，称为过氧化物酶体增殖物激活受体（PPARs）。贝特类药物通过介导PPARα改善致动脉粥样硬化性血脂异常。匹伐他汀是选择性PPARα调节剂（SPPARMα）家族的新成员，其设计目的是比以往的贝特类药物具有更高的PPARα激动活性和选择性。在此，我们旨在研究从非诺贝特转换为匹伐他汀对2型糖尿病患者代谢参数的影响。
我们回顾性选取了从非诺贝特转换为匹伐他汀的2型糖尿病患者，并将转换前的代谢参数与转换后3个月、6个月和12个月的数据进行比较。
我们发现了15例2型糖尿病患者。与基线相比，转换后6个月时血清丙氨酸氨基转移酶显著降低。从非诺贝特转换为匹伐他汀后3个月、6个月和12个月时，估计肾小球滤过率（eGFR）与基线相比显著升高。与基线相比，转换后3个月和6个月时血清尿酸（UA）水平显著升高。转换后我们未观察到其他代谢参数的变化。
我们观察到2型糖尿病患者从非诺贝特转换为匹伐他汀后eGFR和血清UA显著升高。最近的证据表明，2型糖尿病患者eGFR的改善与CVD的发生有益相关。考虑到对eGFR的影响，与非诺贝特相比，匹伐他汀可能更有效地降低CVD。
