临床荟萃 ›› 2022, Vol. 37 ›› Issue (2): 178-181.doi: 10.3969/j.issn.1004-583X.2022.02.017
收稿日期:
2021-07-23
出版日期:
2022-02-20
发布日期:
2022-03-04
通讯作者:
李英
E-mail:Liyinghebei@126.com
Received:
2021-07-23
Online:
2022-02-20
Published:
2022-03-04
摘要:
近年来,随着生活习惯的改变及人口老龄化进程的加快,我国老年糖尿病患者数量逐渐增多。在老年糖尿病患者中,糖尿病肾病(diabetic nephropathy, DN)的发病率极高,已经成为严重影响老年患者生活质量的主要问题之一。然而,DN的发病机制尚不清楚, 有研究发现慢性炎症反应在DN的发生、发展中发挥着重要作用,而肠道菌群失调与DN慢性炎症的发生发展有着密不可分的关系。因此, 明确DN的发病机制、寻找有效的防治措施备受关注,本文就老年DN患者肠道菌群失调的研究进展做一综述。
中图分类号:
杜菲, 李英. 老年糖尿病肾病患者肠道菌群失调的研究进展[J]. 临床荟萃, 2022, 37(2): 178-181.
[1] |
Verma A, Patel AB, Upadhyay A, et al. Credence: Significant victory for diabetic kidney disease[J]. Trends Endocrinol Metab, 2020,31(6):391-393.
doi: 10.1016/j.tem.2020.04.002 URL |
[2] |
Lu CC, Ma KL, Ruan XZ, et al. Intestinal dysbiosis activates renal renin-angiotensin system contributing to incipient diabetic nephropathy[J]. Int J Med Sci, 2018,15(8):816-822.
doi: 10.7150/ijms.25543 URL |
[3] | 张青, 刘旭生, 张蕾. 糖尿病肾脏病患者肠道菌群紊乱的发生发展机制[J]. 世界科学技术-中医药现代化, 2020,22(9):3235-3240. |
[4] |
Nallu A, Sharma S, Ramezani A, et al. Gut microbiome in chronic kidney disease: Challenges and opportunities[J]. Transl Res. 2017,179:24-37.
doi: 10.1016/j.trsl.2016.04.007 URL |
[5] | 李雷, 杨云梅, 吴月. 老年2型糖尿病患者肠道菌群多样性及其炎症因子与胰岛素抵抗的相关性研究[J]. 中华危重症医学杂志 (电子版), 2018,11(5):316-321. |
[6] |
Xu KY, Xia GH, Lu JQ, et al. Impaired renal function and dysbiosis of gut microbiota contribute to increased trimethylamine-N-oxide in chronic kidney disease patients[J]. Sci Rep, 2017,7(1):1445.
doi: 10.1038/s41598-017-01387-y URL |
[7] |
Felizardo RJF, Castoldi A, Andrade-Oliveira V, et al. The microbiota and chronic kidney diseases: A double-edged sword[J]. Clin Transl Immunol, 2016,5(6):e86.
doi: 10.1038/cti.2016.36 URL |
[8] | Chen Z, Zhu S, Xu G. Targeting gut microbiota: A potential promising therapy for diabetic kidney disease[J]. Am J Transl Res, 2016,8(10):4009-4016. |
[9] |
Pluznick JL. Gut microbiota in renal physiology: Focus on short-chain fatty acids and their receptors[J]. Kidney Int, 2016,90(6):1191-1198.
doi: 10.1016/j.kint.2016.06.033 URL |
[10] |
Ikee R, Sasaki N, Yasuda T, et al. Chronic kidney disease, gut dysbiosis, and Constipation: A Burdensome triplet[J]. Microorganisms, 2020,8(12):1862.
doi: 10.3390/microorganisms8121862 URL |
[11] |
Zhao J, Ning X, Liu B, et al. Specific alterations in gut microbiota in patients with chronic kidney disease: An updated systematic review[J]. Ren Fail, 2021,43(1):102-112.
doi: 10.1080/0886022X.2020.1864404 pmid: 33406960 |
[12] |
Muskiet MH, Smits MM, Morsink LM, et al. The gut-renal axis: Do incretin-based agents confer renoprotection in diabetes?[J]. Nat Rev Nephrol, 2014,10(2):88-103.
doi: 10.1038/nrneph.2013.272 pmid: 24375052 |
[13] |
Kim YA, Keogh JB, Clifton PM. Probiotics, prebiotics, synbiotics and insulin sensitivity[J]. Nutr Res Rev, 2018,31(1):35-51.
doi: 10.1017/S095442241700018X pmid: 29037268 |
[14] |
Cani PD, Bibiloni R, Knauf C, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice[J]. Diabetes, 2008,57(6):1470-1481.
doi: 10.2337/db07-1403 URL |
[15] |
Devaraj S, Dasu MR, Park SH, et al. Increased levels of ligands of Toll-like receptors 2 and 4 in type 1 diabetes[J]. Diabetologia, 2009,52(8):1665-1668.
doi: 10.1007/s00125-009-1394-8 pmid: 19455302 |
[16] |
Devaraj S, Dasu MR, Rockwood J, et al. Increased toll-like receptor (TLR) 2 and TLR4 expression in monocytes from patients with type 1 diabetes: Further evidence of a proinflammatory state[J]. J Clin Endocrinol Metab, 2018,93(2):578-583.
doi: 10.1210/jc.2007-2185 URL |
[17] |
Liang H, Hussey SE, Sanchez-Avila A, et al. Effect of lipopolysaccharide on inflammation and insulin action in human muscle[J]. PLoS One, 2013,8(5):e63983.
doi: 10.1371/journal.pone.0063983 URL |
[18] | Chen Z, Zhu S, Xu G. Targeting gut microbiota: A potential promising therapy for diabetic kidney disease[J]. Am J Transl Res, 2016,8(10):4009-4016. |
[19] |
Lafferty RA, Flatt PR, Irwin N. Emerging therapeutic potential for peptide YY for obesity-diabetes[J]. Peptides, 2018,100:269-274.
doi: S0196-9781(17)30336-4 pmid: 29412828 |
[20] |
Shen L, Ao L, Xu H, et al. Poor short-term glycemic control in patients with type 2 diabetes impairs the intestinal mucosal barrier: A prospective, single-center, observational study[J]. BMC Endocr Disord, 2019,19(1):29.
doi: 10.1186/s12902-019-0354-7 URL |
[21] | Wu TK, Lim PS, Jin JS, et al. Impaired gut epithelial tight junction expression in hemodialysis patients complicated with intradialytic hypotension[J]. Biomed Res Int, 2018 16, 2018: 2670312. |
[22] |
Atoh K, Itoh H, Haneda M. Serum indoxyl sulfate levels in patients with diabetic nephropathy: Relation to renal function[J]. Diabetes Res Clin Pract, 2009,83(2):220-226.
doi: 10.1016/j.diabres.2008.09.053 URL |
[23] |
Sun CY, Hsu HH, Wu MS.p-Cresol sulfate and indoxyl sulfate induce similar cellular inflammatory gene expressions in cultured proximal renal tubular cells[J]. Nephrol Dial Transplant, 2013,28(1):70-78.
doi: 10.1093/ndt/gfs133 URL |
[24] |
Bolati D, Shimizu H, Yisireyili M, et al. Indoxyl sulfate, a uremic toxin, downregulates renal expression of Nrf2 through activation of NF-κB[J]. BMC Nephrol, 2013,14:56.
doi: 10.1186/1471-2369-14-56 URL |
[25] |
Adesso S, Magnus T, Cuzzocrea S, et al. Indoxyl sulfate affects glial function increasing oxidative stress and neuroinflammation in chronic kidney disease: Interaction between astrocytes and microglia[J]. Front Pharmacol, 2017,8:370.
doi: 10.3389/fphar.2017.00370 URL |
[26] |
Sun CY, Chang SC, Wu MS. Uremic toxins induce kidney fibrosis by activating intrarenal renin-angiotensin-aldosterone system associated epithelial-to-mesenchymal transition[J]. PLoS One, 2012,7(3):e34026.
doi: 10.1371/journal.pone.0034026 URL |
[27] |
Fernandes ALF, Borges NA, Black AP, et al. Dietary intake of tyrosine and phenylalanine, and p-cresyl sulfate plasma levels in non-dialyzed patients witchronic kidney disease[J]. J Bras Nefrol, 2020,42(3):307-314.
doi: 10.1590/2175-8239-jbn-2018-0214 URL |
[28] |
Niewczas MA, Sirich TL, Mathew AV, et al. Uremic solutes and risk of end-stage renal disease in type 2 diabetes: Metabolomic study[J]. Kidney Int, 2014,85(5):1214-1224.
doi: 10.1038/ki.2013.497 pmid: 24429397 |
[29] |
Watanabe H, Miyamoto Y, Honda D, et al. p-Cresyl sulfate causes renal tubular cell damage by inducing oxidative stress by activation of NADPH oxidas[J]. Kidney Int, 2013,83(4):582-592.
doi: 10.1038/ki.2012.448 pmid: 23325087 |
[30] |
Gruppen EG, Garcia E, Connelly MA, et al. TMAO is associated with mortality: Impact of modestly impaired renal function[J]. Sci Rep, 2017,7(1):13781.
doi: 10.1038/s41598-017-13739-9 pmid: 29061990 |
[31] | Ma G, Pan B, Chen Y, et al. Trimethylamine N-oxide in atherogenesis: Impairing endothelial self-repair capacity and enhancing monocyte adhesion[J]. Biosci Rep, 2017,37(2):BSR20160244. |
[32] | Oellgaard J, Winther SA, Hansen TS, et al. Trimethylamine N-oxide(TMAO) as a new potential therapeutic target for insulin resistance and cancer[J]. Curr Pharm Des, 2017,23(25):3699-3712. |
[33] |
Sun G, Yin Z, Liu N, et al. Gut microbial metabolite TMAO contributes to renal dysfunction in a mouse model of diet-induced obesity[J]. Biochem Biophys Res Commun, 2017,493(2):964-970.
doi: 10.1016/j.bbrc.2017.09.108 URL |
[34] |
Zhang W, Miikeda A, Zuckerman J, et al. Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice[J]. Sci Rep, 2021,11(1):518.
doi: 10.1038/s41598-020-80063-0 URL |
[35] |
Gupta N, Buffa JA, Roberts AB, et al. Targeted inhibition of gut microbial trimethylamine N-oxide production reduces renal tubulointerstitial fibrosis and functional impairment in a murine model of chronic kidney disease[J]. Arterioscler Thromb Vasc Biol, 2020,40(5):1239-1255.
doi: 10.1161/ATVBAHA.120.314139 URL |
[36] |
Koppe L, Mafra D, Fouque D. Probiotics and chronic kidney disease[J]. Kidney Int, 2015,88(5):958-966.
doi: 10.1038/ki.2015.255 URL |
[37] |
Jia L, Dong X, Li X, et al. Benefits of resistant starch type 2 for patients with end-stage renal disease under maintenance hemodialysis: A systematic review and meta-analysis[J]. Int J Med Sci, 2021,18(3):811-820.
doi: 10.7150/ijms.51484 URL |
[38] |
Koh GY, Rowling MJ. Resistant starch as a novel dietary strategy to maintain kidney health in diabetes mellitus[J]. Nutr Rev, 2017,75(5):350-360.
doi: 10.1093/nutrit/nux006 URL |
[39] |
Liu WC, Tomino Y, Lu KC. Impacts of Indoxyl Sulfate and p-Cresol Sulfate on Chronic Kidney Disease and Mitigating Effects of AST-120[J]. Toxins (Basel), 2018,10(9):367.
doi: 10.3390/toxins10090367 URL |
[40] |
Ramezani A, Massy ZA, Meijers B, et al. Role of the gut microbiome in uremia: A potential therapeutic target[J]. Am J Kidney Dis, 2016,67(3):483-498.
doi: 10.1053/j.ajkd.2015.09.027 pmid: 26590448 |
[41] |
Li DY, Tang WHW. Contributory role of gut microbiota and their metabolites toward cardiovascular complications in chronic kidney disease[J]. Semin Nephrol, 2018,38(2):193-205.
doi: 10.1016/j.semnephrol.2018.01.008 URL |
[42] |
Wu J, Zhang YY, Guo L, et al. Bupleurum polysaccharides attenuates lipopolysaccharide-induced inflammation via modulating Toll-like receptor 4 signaling[J]. PLoS One, 2013,8(10):e78051.
doi: 10.1371/journal.pone.0078051 URL |
[43] |
Pan L, Weng H, Li H, et al. Therapeutic effects of bupleurum polysaccharides in streptozotocin induced diabetic mice[J]. PLoS One, 2015,10(7):e0133212.
doi: 10.1371/journal.pone.0133212 URL |
[44] |
Brandt LJ, Aroniadis OC. An overview of fecal microbiota transplantation: Techniques, indications, and outcomes[J]. Gastrointest Endosc, 2013,78(2):240-249.
doi: 10.1016/j.gie.2013.03.1329 URL |
[45] |
Zhou D, Pan Q, Shen F, et al. Total fecal microbiota transplantation alleviates high-fat diet-induced steatohepatitis in mice via beneficial regulation of gut microbiota[J]. Sci Rep, 2017,7(1):1529.
doi: 10.1038/s41598-017-01751-y pmid: 28484247 |
[1] | 张晓璐, 李红山. 自身免疫性肝炎发病机制研究进展——聚焦“肠道菌群与免疫系统相互作用”[J]. 临床荟萃, 2024, 39(2): 177-182. |
[2] | 杨小雄, 杨帆, 魏小果. 肠-微生物群-肝轴与代谢相关脂肪性肝病的研究进展[J]. 临床荟萃, 2023, 38(6): 559-563. |
[3] | 陈婷, 刘金彦. 中药靶向PI3K/Akt/mTOR通路调节自噬在糖尿病肾脏病中的研究进展[J]. 临床荟萃, 2023, 38(6): 564-568. |
[4] | 易静静, 圈启芳, 马婕. 调节小胶质细胞反应性:糖尿病视网膜病变新见解[J]. 临床荟萃, 2023, 38(4): 364-368. |
[5] | 李会芳, 苗霞. 甲状腺激素水平对2型糖尿病肾脏病风险的预测[J]. 临床荟萃, 2023, 38(2): 137-142. |
[6] | 谢少为, 吕小涵, 董艳红, 吕佩源. 抗炎细胞因子在阿尔茨海默病中的研究进展[J]. 临床荟萃, 2023, 38(2): 185-188. |
[7] | 代菁, 陈华茜. 血液透析患者自发性肾破裂1例并文献复习[J]. 临床荟萃, 2023, 38(12): 1107-1111. |
[8] | 王思源, 王利, 温新然, 李小青. 新型冠状病毒感染后儿童多系统炎症综合征2例并文献复习[J]. 临床荟萃, 2023, 38(12): 1112-1116. |
[9] | 李志勇. 超声诊断短暂颈动脉周围炎症综合征1例并文献复习[J]. 临床荟萃, 2023, 38(11): 1027-1030. |
[10] | 张娟, 田茂露, 查艳. 维持性血液透析患者的微炎症状态与促红细胞生成素低反应性贫血[J]. 临床荟萃, 2023, 38(10): 949-953. |
[11] | 王翠, 林昊, 武萍萍, 张雅丽, 任建, 徐婷, 董国玉, 宰国田. 2型糖尿病患者高同型半胱氨酸血症与早期肾脏疾病的相关性[J]. 临床荟萃, 2023, 38(1): 42-45. |
[12] | 姚瑶, 褚敏. 糖尿病肾病患者认知功能障碍与血清β淀粉样蛋白的关系[J]. 临床荟萃, 2022, 37(9): 813-816. |
[13] | 王晶霞, 汤灵玲. 肠道微生物群疗法防治复发性艰难梭菌感染研究进展[J]. 临床荟萃, 2022, 37(8): 759-763. |
[14] | 轩晓倩, 赵君慧, 杨小茜. 炎性指标在非小细胞肺癌患者预后中的临床意义[J]. 临床荟萃, 2022, 37(7): 663-667. |
[15] | 王杰, 陈宝昌, 黄嘉瑜, 孟金凤, 李尚彬, 闫伟宸, 赵倩, 李娇, 任常军. 新生儿脑损伤与围生期感染关联性的Meta分析[J]. 临床荟萃, 2022, 37(6): 497-503. |
阅读次数 | ||||||
全文 |
|
|||||
摘要 |
|
|||||