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作 者:白璐[1] 李青霞 冯一卓 刘雪倩 刘若琪 曲卓敏 赵凌霞[1] Bai Lu;Li Qingxia;Feng Yizhuo;Liu Xueqian;Liu(Ruoqi,Qu Zhuomin,Zhao Lingxia.Department of Endocrinology,Third Hospital of Shanxi Medical University,Shanxi Bethune Hospital,Shanxi Academy of Medical Sciences,Tongji Shanxi Hospital,Taiyuan,030032,China)
机构地区:[1]山西医科大学第三医院(山西白求恩医院山西医学科学院同济山西医院)内分泌科,太原030032
出 处:《中华临床医师杂志(电子版)》2024年第3期303-308,共6页Chinese Journal of Clinicians(Electronic Edition)
基 金:山西省自然科学基金项目(202103021224356)。
摘 要:糖尿病肾病是糖尿病最常见的慢性微血管并发症之一,目前常规治疗并不能完全延缓其发生和发展。因此,开发新的药物治疗糖尿病肾病并改善肾功能已经成为一个活跃的研究领域。近年来研究发现,在糖尿病肾病患者体内产丁酸盐菌丰度显著降低,丁酸盐生成减少。丁酸盐作为肠-肾轴的关键递质,通过激活G蛋白偶联受体、抑制组蛋白去乙酰化酶、调控非编码RNA的表达、诱导组蛋白丁酰化、调节细胞自噬等途径改善和减轻糖尿病肾脏损伤。该综述旨在探讨上述机制介导的丁酸盐改善糖尿病肾脏损伤作用,以及恢复肠道丁酸盐水平的相关治疗策略,为糖尿病肾病的发病机制和治疗研究提供参考。Diabetic kidney disease is one of the most common chronic microvascular complications of diabetes mellitus,and current conventional treatments can not completely delay its onset and progression.Therefore,the development of new drugs to treat diabetic kidney disease and improve renal function has become an active area of research.In recent years,it has been found that the abundance of butyrate-producing bacteria is significantly reduced in patients with diabetic kidney disease,and butyrate production is reduced.As a key transmitter of the gut-renal axis,butyrate ameliorates and attenuates diabetic kidney injury by activating G protein-coupled receptors,inhibiting histone deacetylase,regulating non-coding RNA expression,inducing histone butyrylation,and regulating cellular autophagy.The aim of this review is to explore the role of butyrate in ameliorating diabetic kidney injury and the related therapeutic strategies for restoring intestinal butyrate levels,which will provide a reference for the study of the pathogenesis and treatment of diabetic kidney disease.
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