轻度持续生理性高血糖损害正常糖耐量个体的肝胰岛素敏感性

Mild sustained physiological hyperglycemia impairs hepatic insulin sensitivity in healthy individuals with normal glucose tolerance

研究已表明慢性高血糖会加重骨骼肌胰岛素抵抗并损害β细胞功能,然而持续生理性高血糖对肝胰岛素敏感性的效果尚未明确。最近,Journal of Clinical Endocrinology&Metabolism杂志发表了1篇题为《轻度生理性高血糖在正常糖耐量受试者中诱导肝胰岛素抵抗》的论著[Tripathy D,Merovci A,Basu R,et al.J Clin Endocrinol Metab,2019,104(7):2842-2850]。在获得原文杂志的授权后,本文对该文进行了中文编译。该研究通过三阶段高胰岛素正葡萄糖钳夹试验在16名健康个体中检测了持续生理性高血糖对内源性葡萄糖生成的影响。结果显示,在正常糖耐量个体中,即使只持续48h的生理性高血糖也会增加基础肝葡萄糖生成率并诱导肝胰岛素抵抗,提示糖毒性对2型糖尿病患者肝糖生成增加起作用。

Previous studies have shown that chronic hyperglycemia exacerbates skeletal muscle insulin resistance and worsensβ-cell function.However,the effect of sustained physiologic hyperglycemia on hepatic insulin sensitivity stays unclear.This paper is the Chinese translation of"Mild physiologic hyperglycemia induces hepatic insulin resistance in healthy normal glucose-tolerant participants",published on"Journal of Clinical Endocrinology&Metabolism"[Tripathy D,Merovci A,Basu R,et al.J Clin Endocrinol Metab,2019,104(7):2842-2850]after obtaining the copyright of the original journal.This study examined the effect of sustained physiologic hyperglycemia on endogenous glucose production(EGP)in 16 healthy individuals with three-step hyperinsulinemic euglycemic clamp.The results showed that sustained physiologic hyperglycemia for only 48 hours increased the rate of basal hepatic glucose production and induced hepatic insulin resistance in healthy persons with normal glucose tolerance,indicating the role of glucotoxicity in the increase of hepatic glucose production in type 2 diabetes.