Department of Internal Medicine, Korea University Guro Hospital, Seoul, Korea.
Department of Biostatistics, Korea University College of Medicine, Seoul, Korea.
Clin Exp Pharmacol Physiol. 2020 Jun;47(6):947-954. doi: 10.1111/1440-1681.13272. Epub 2020 Feb 26.
Several studies suggest the higher vulnerability of individuals with lower low-density lipoprotein cholesterol (LDL-C) levels to diabetes mellitus. However, the discordance between high and low baseline LDL-C levels shown by statin-induced insulin resistance is not fully understood. This study aimed to explore the relationship between baseline LDL-C levels and the risk of statin-induced insulin resistance during statin therapy. In total, 2660 (451 with dyslipidemia and 2209 without dyslipidemia) consecutive patients were enrolled. Their baseline clinical data were adjusted using a propensity score matching analysis, using the logistic regression model. Insulin resistance index was based on the homeostatic model assessment-insulin resistance (HOMA-IR) and was monitored for a median of 2 years. Among the individuals who received statin therapy, those with and without dyslipidemia showed significantly decreased LDL-C levels (all P < .0001) and significantly increased fasting plasma insulin levels (Δ = +24.1%, P = .0230; Δ = +30.1%, P < .0001); however, their glycated haemoglobin A1c and fasting blood glucose levels did not change (all P > .05). Although HOMA-IR was positively associated with statin therapy in individuals with and without dyslipidemia, statistically significant difference during follow-ups was observed only in individuals without dyslipidemia (Δ = +15.6%, P = .1609; Δ = 24.0%; P = .0001). Insulin resistance was higher in statin users without baseline dyslipidemia than in those with dyslipidemia. Thus, statin therapy could increase the risk of statin-induced insulin resistance in individuals with normal baseline cholesterol levels.
一些研究表明，低密度脂蛋白胆固醇（LDL-C）水平较低的个体更容易患糖尿病。然而，他汀类药物引起的胰岛素抵抗所表现出的高基线和低基线 LDL-C 水平之间的不匹配尚未完全被理解。本研究旨在探讨他汀类药物治疗期间基线 LDL-C 水平与他汀类药物诱导的胰岛素抵抗风险之间的关系。共有 2660 名（451 名血脂异常，2209 名血脂正常）连续患者入组。使用倾向评分匹配分析调整了他们的基线临床数据，使用逻辑回归模型。胰岛素抵抗指数基于稳态模型评估-胰岛素抵抗（HOMA-IR），并监测中位数为 2 年。在接受他汀类药物治疗的患者中，血脂异常和无血脂异常患者的 LDL-C 水平均显著降低（均 P <.0001），空腹血浆胰岛素水平显著升高（Δ=+24.1%，P=.0230；Δ=+30.1%，P <.0001）；然而，他们的糖化血红蛋白 A1c 和空腹血糖水平没有变化（均 P >.05）。尽管他汀类药物治疗与血脂异常和无血脂异常患者的 HOMA-IR 呈正相关，但仅在无血脂异常患者中观察到随访期间的统计学显著差异（Δ=+15.6%，P=.1609；Δ=24.0%；P=.0001）。与基线血脂异常的他汀类药物使用者相比，无基线血脂异常的他汀类药物使用者的胰岛素抵抗更高。因此，他汀类药物治疗可能会增加正常基线胆固醇水平个体发生他汀类药物诱导的胰岛素抵抗的风险。
