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SGLT-1 特异性抑制可改善腺嘌呤诱导的肾衰竭小鼠的肾衰竭并改变肠道微生物群落。

SGLT-1-specific inhibition ameliorates renal failure and alters the gut microbial community in mice with adenine-induced renal failure.

机构信息

Department of Medical Science, Tohoku University Graduate School of Biomedical Engineering, Sendai, Japan.

Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

出版信息

Physiol Rep. 2021 Dec;9(24):e15092. doi: 10.14814/phy2.15092.

Abstract

Sodium-dependent glucose cotransporters (SGLTs) have attracted considerable attention as new targets for type 2 diabetes mellitus. In the kidney, SGLT2 is the major glucose uptake transporter in the proximal tubules, and inhibition of SGLT2 in the proximal tubules shows renoprotective effects. On the other hand, SGLT1 plays a role in glucose absorption from the gastrointestinal tract, and the relationship between SGLT1 inhibition in the gut and renal function remains unclear. Here, we examined the effect of SGL5213, a novel and potent intestinal SGLT1 inhibitor, in a renal failure (RF) model. SGL5213 improved renal function and reduced gut-derived uremic toxins (phenyl sulfate and trimethylamine-N-oxide) in an adenine-induced RF model. Histological analysis revealed that SGL5213 ameliorated renal fibrosis and inflammation. SGL5213 also reduced gut inflammation and fibrosis in the ileum, which is a primary target of SGL5213. Examination of the gut microbiota community revealed that the Firmicutes/Bacteroidetes ratio, which suggests gut dysbiosis, was increased in RF and SGL5213 rebalanced the ratio by increasing Bacteroidetes and reducing Firmicutes. At the genus level, Allobaculum (a major component of Erysipelotrichaceae) was significantly increased in the RF group, and this increase was canceled by SGL5213. We also measured the effect of SGL5213 on bacterial phenol-producing enzymes that catalyze tyrosine into phenol, following the reduction of phenyl sulfate, which is a novel marker and a therapeutic target for diabetic kidney disease DKD. We found that the enzyme inhibition was less potent, suggesting that the change in the microbial community and the reduction of uremic toxins may be related to the renoprotective effect of SGL5213. Because SGL5213 is a low-absorbable SGLT1 inhibitor, these data suggest that the gastrointestinal inhibition of SGLT1 is also a target for chronic kidney diseases.

摘要

钠-葡萄糖协同转运蛋白(SGLTs)作为 2 型糖尿病的新靶点引起了广泛关注。在肾脏中,SGLT2 是近端小管中主要的葡萄糖摄取转运体,抑制近端小管中的 SGLT2 具有肾脏保护作用。另一方面,SGLT1 在胃肠道对葡萄糖的吸收中起作用,而肠道中 SGLT1 抑制与肾功能之间的关系尚不清楚。在这里,我们在肾衰竭(RF)模型中检查了新型强效肠道 SGLT1 抑制剂 SGL5213 的作用。SGL5213 可改善腺嘌呤诱导的 RF 模型中的肾功能并降低肠道来源的尿毒症毒素(对苯磺酸和三甲胺 N-氧化物)。组织学分析表明,SGL5213 可改善肾纤维化和炎症。SGL5213 还可减轻回肠中的肠道炎症和纤维化,回肠是 SGL5213 的主要靶标。对肠道微生物群落的检查表明,拟杆菌/厚壁菌比值(提示肠道菌群失调)在 RF 中增加,SGL5213 通过增加拟杆菌和减少厚壁菌来重新平衡该比值。在属水平上, RF 组中的 Allobaculum(Erysipelotrichaceae 的主要成分)显着增加,而 SGL5213 可消除这种增加。我们还测量了 SGL5213 对细菌苯酚产生酶的影响,这些酶可催化酪氨酸转化为苯酚,这是糖尿病肾病(DKD)的新型标志物和治疗靶标。我们发现,酶抑制作用较弱,表明微生物群落的变化和尿毒症毒素的减少可能与 SGL5213 的肾脏保护作用有关。由于 SGL5213 是一种低吸收率的 SGLT1 抑制剂,因此这些数据表明,SGLT1 的胃肠道抑制也是慢性肾脏病的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b9a/8683788/0af0e5bb03c4/PHY2-9-e15092-g006.jpg

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