Novel hypothesis to explain why SGLT2 inhibitors inhibit only 30-50% of filtered glucose load in humans.

Novel hypothesis to explain why SGLT2 inhibitors inhibit only 30-50% of filtered glucose load in humans.
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DOI:
10.2337/db13-0604
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发表时间:
2013-10
期刊:
影响因子:
7.7
通讯作者:
Norton L
Norton L
中科院分区:
医学1区
文献类型:
--
作者:
Abdul-Ghani MA;DeFronzo RA;Norton L

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钠-葡萄糖协同转运蛋白2(SGLT 2)抑制剂是一类新型抗糖尿病药物,该类药物正处于治疗2型糖尿病(T2DM)的不同临床开发阶段。普遍认为SGLT 2负责> 80%的肾滤过葡萄糖负荷重吸收。然而,最大剂量的SGLT 2抑制剂未能抑制> 50%的过滤葡萄糖负荷。由于这组药物的临床疗效完全取决于产生的糖尿量,因此了解SGLT 2抑制剂抑制<50%滤过葡萄糖负荷的原因非常重要。在这个角度来看,我们提供了一个新的假设,解释这个明显的困惑,并讨论了一些固有的临床意义,在这个假设。
Inhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabetes drugs, and members of this class are under various stages of clinical development for the management of type 2 diabetes mellitus (T2DM). It is widely accepted that SGLT2 is responsible for >80% of the reabsorption of the renal filtered glucose load. However, maximal doses of SGLT2 inhibitors fail to inhibit >50% of the filtered glucose load. Because the clinical efficacy of this group of drugs is entirely dependent on the amount of glucosuria produced, it is important to understand why SGLT2 inhibitors inhibit <50% of the filtered glucose load. In this Perspective, we provide a novel hypothesis that explains this apparent puzzle and discuss some of the clinical implications inherent in this hypothesis.
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