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SGLT2 knockout prevents hyperglycemia and is associated with reduced pancreatic β-cell death in genetically obese mice

机译：SGLT2敲除可防止高血糖，并且与遗传肥胖小鼠的胰腺β细胞死亡降低有关

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ABSTRACT: Inhibition of the sodium-glucose co-transporter type 2 (SGLT2) has received growing acceptance as a novel, safe and effective means to improve glycemic control in patients with type 2 diabetes. Inhibition of SGLT2 lowers the renal glucose threshold and reduces plasma glucose by promoting glucose excretion in urine. Both animal studies and clinical trials in man suggest that SGLT2 inhibition has the potential to improve pancreatic β-cell function by reducing glucose toxicity. However, there is limited data exploring how reducing glucotoxicity via SGLT2 inhibition affects rates of β-cell proliferation and death throughout life in the context of insulin resistance and type 2 diabetes. SGLT2?/? mice were backcrossed to the db/db strain to produce littermate control db/db-SGLT2+/+ and experimental db/db-SGLT2?/? mice. Mice were euthanized at 5, 12 and 20 weeks of age to collect plasma for glucose, insulin, lipid and cytokine measures, and pancreata for histological analysis including determination of β-cell mass and rates of proliferation and death. SGLT2 deletion in db/db mice reduced plasma glucose as early as 5 weeks of age and continued throughout life without changes in plasma lipids or cytokines. Reduced plasma glucose levels occurred in parallel with an increase in the relative β-cell volume and reduced frequency of β-cell death, and no apparent change in rates of β-cell proliferation. These data add to a growing body of evidence demonstrating that improved glycemic control achieved through SGLT2 inhibition can preserve β-cell function and endogenous insulin secretion by reducing glucose toxicity and rates of β-cell death. ? 2018, ? 2018 The Authors. Published with license byTaylor & Francis.
机译：摘要：抑制钠 - 葡萄糖共转运蛋白2（SGLT2）的抑制因其在2型糖尿病患者中提高血糖控制的新颖，安全有效的手段而产生的验收。抑制SGLT2降低了肾葡萄糖阈值并通过促进尿液中的葡萄糖排泄来减少血浆葡萄糖。人类的动物研究和临床试验表明，SGLT2抑制具有通过降低葡萄糖毒性来改善胰腺β细胞功能的潜力。然而，存在有限的数据探讨通过SGLT2抑制减少葡萄酸毒性的影响影响胰岛素抵抗和2型糖尿病在整个生命中的β细胞增殖和死亡率。 SGLT2？/？将小鼠恢复到DB / DB菌株中以产生偶体对照DB / DB-SGLT2 + / +和实验DB / DB-SGLT2？/？老鼠。将小鼠在5,12和20周安乐死，以收集葡萄糖，胰岛素，脂质和细胞因子措施的血浆，以及用于组织学分析的胰腺癌，包括测定β细胞质量和增殖和死亡率的测定。 SGLT2在DB / DB小鼠中删除血浆葡萄糖早5周减少，并且在整个寿命中持续而不发生血浆脂质或细胞因子的变化。降低血浆葡萄糖水平与相对β细胞体积的增加和β细胞死亡的频率降低，并且没有明显变化的β细胞增殖。这些数据增加了越来越多的证据，证明通过SGLT2抑制所实现的改善血糖控制可以通过降低葡萄糖毒性和β细胞死亡率来保护β细胞功能和内源性胰岛素分泌。还2018年，？ 2018年作者。发布Bytaylor＆Francis许可证。

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