[1]傅一星,罗朋立.胰岛素抵抗与肾损伤的机制[J].医学信息,2020,33(24):45-48.[doi:10.3969/j.issn.1006-1959.2020.24.013]
 FU Yi-xing,LUO Peng-li.Mechanism of Insulin Resistance and Kidney Injury[J].Medical Information,2020,33(24):45-48.[doi:10.3969/j.issn.1006-1959.2020.24.013]
点击复制

胰岛素抵抗与肾损伤的机制()
分享到:

医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
33卷
期数:
2020年24期
页码:
45-48
栏目:
综述
出版日期:
2020-12-15

文章信息/Info

Title:
Mechanism of Insulin Resistance and Kidney Injury
文章编号:
1006-1959(2020)24-0045-04
作者:
傅一星罗朋立
青海大学研究生院,青海 西宁 810000
Author(s):
FU Yi-xingLUO Peng-li
Graduate School of Qinghai University,Xining 810000,Qinghai,China
关键词:
胰岛素抵抗肾损伤胰岛素信号通路调节因子代谢
Keywords:
Insulin resistanceKidney injuryInsulin signaling pathwayRegulatorsMetabolism
分类号:
R692
DOI:
10.3969/j.issn.1006-1959.2020.24.013
文献标志码:
A
摘要:
胰岛素抵抗主要表现为机体对胰岛素敏感性下降。胰岛素受体广泛表达于肾脏固有细胞,故胰岛素抵抗与肾功能损伤关系密切,胰岛素抵抗可通过直接损伤PI3K-AKT信号传导通路,调节如SIRTs、SHIP2、PTEN及PTP1B等相关因子,影响自噬活性来导致足细胞发生结构及功能改变;通过影响肾小管megalin和cubilin蛋白、钠-葡萄糖协同转运蛋白及电碳酸氢钠共转运蛋白1等的表达从而导致白蛋白、葡萄糖、钠及其他离子的重吸收受损;加重系膜细胞及内皮细胞的损伤。本文现就胰岛素抵抗对足细胞、系膜细胞、肾小管细胞、内皮细胞均有损伤作用进行综述。
Abstract:
Insulin resistance is mainly manifested as the body’s decreased sensitivity to insulin. Insulin receptors are widely expressed in the intrinsic cells of the kidney, so insulin resistance is closely related to renal function damage. Insulin resistance can directly damage PI3K-AKT signaling pathways and regulate related factors such as SIRTs, SHIP2, PTEN and PTP1B.Influencing autophagy activity to cause structural and functional changes in podocytes; by affecting the expression of renal tubule megalin and cubilin proteins, sodium-glucose cotransporter and sodium bicarbonate cotransporter 1, resulting in albumin, glucose, sodium and reabsorption of other ions is impaired; it increases the damage of mesangial cells and endothelial cells. This article reviews the effects of insulin resistance on podocytes, mesangial cells, renal tubular cells, and endothelial cells.

参考文献/References:

[1]Artunc F,Schleicher E,Weigert C,et al.The impact of insulin resistance on the kidney and vasculature[J].Nat Rev Nephrol,2016,12(12):721-737. [2]Singh S,Sharma R,Kumari M,et al.Insulin receptors in the kidneys in health and disease[J].World J Nephrol,2019,8(1):11-22. [3]Conte C,Epstein S,Napoli N.Insulin resistance and bone: a biological partnership[J].Acta Diabetol,2018,55(4):305-314. [4]Lay AC,Hurcombe JA,Betin VMS,et al.Prolonged exposure of mouse and human podocytes to insulin induces insulin resistance through lysosomal and proteasomal degradation of the insulin receptor[J].Diabetologia,2017,60(11):2299-2311. [5]Garner KL,Betin VMS,Pinto V,et al.Enhanced insulin receptor, but not PI3K, signalling protects podocytes from ER stress[J].Sci Rep,2018,8(1):3902. [6]Rogacka D,Piwkowska A,Audzeyenka I,et al.SIRT1-AMPK crosstalk is involved in high glucose-dependent impairment of insulin responsiveness in primary rat podocytes[J].Exp Cell Res, 2016,349(2):328-338. [7]Rogacka D,Audzeyenka I,Rych?owski M,et al.Metformin overcomes high glucose-induced insulin resistance of podocytes by pleiotropic effects on SIRT1 and AMPK[J].Biochim Biophys Acta Mol Basis Dis,2018,1864(1):115-125. [8]Yang D,Livingston MJ,Liu Z,et al.Autophagy in diabetic kidney disease: regulation, pathological role and therapeutic potential[J].Cell Mol Life Sci,2018,75(4):669-688. [9]Polianskyte-Prause Z,Tolvanen TA,Lindfors S,et al.Metformin increases glucose uptake and acts renoprotectively by reducing SHIP2 activity[J].FASEB J,2019,33(2):2858-2869. [10]Rogacka D,Piwkowska A,Audzeyenka I,et al.Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes[J].Int J Biochem Cell Biol,2014(51):120-130. [11]Garner KL,Betin VMS,Pinto V,et al.Enhanced insulin receptor, but not PI3K, signalling protects podocytes from ER stress[J].Sci Rep,2018,8(1):3902. [12]Geraldes P.Protein phosphatases and podocyte function[J].Curr Opin Nephrol Hypertens,2018,27(1):49-55. [13]Ito Y,Hsu MF,Bettaieb A,et al.Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury[J].Metabolism,2017(76):56-69. [14]Matulewicz N,Karczewska-Kupczewska M.Insulin resistance and chronic inflammation[J].Postepy Hig Med Dosw (Online),2016(70):1245-1258. [15]Du P,Fan B,Han H,et al.NOD2 promotes renal injury by exacerbating inflammation and podocyte insulin resistance in diabetic nephropathy[J].Kidney Int,2013,84(2):265-276. [16]Mohamed R,Jayakumar C,Chen F,et al.Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis[J].J Am Soc Nephrol,2016,27(3):745-765. [17]Levine B,Ranganathan R.Autophagy: Snapshot of the network[J].Nature,2010,466(7302):38-40. [18]Xu Y,Zhou Q,Xin W,et al.Autophagy downregulation contributes to insulin resistance mediated injury in insulin receptor knockout podocytes in vitro[J].Peer J,2016(4):e1888. [19]Xin W,Li Z,Xu Y,et al.Autophagy protects human podocytes from high glucose-induced injury by preventing insulin resistance[J].Metabolism,2016,65(9):1307-1315. [20]Audzeyenka I,Rogacka D,Piwkowska A,et al.Viability of primary cultured podocytes is associated with extracellular highglucose-dependent autophagy downregulation[J].Mol Cell Biochem,2017,430(1-2):11-19. [21]Zhan X,Yan C,Chen Y,et al.Celastrol antagonizes high glucose-evoked podocyte injury, inflammation and insulin resistance by restoring the HO-1-mediated autophagy pathway[J].Mol Immunol,2018(104):61-68. [22]Hurcombe JA,Lay AC,Ni L,et al.Podocyte GSK3α is important for autophagy and its loss detrimental for glomerular function[J].FASEB Bioadv,2019,1(8):498-510. [23]Cao AL,Wang L,Chen X,et al.Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy[J].Lab Invest,2016,96(6):610-622. [24]Li Z,Yuan Y,Meng Y,et al.Autophagy upregulation ameliorates cell injury in Sequestosome 1 knockout podocytes in vitro[J].Biochem Biophys Res Commun,2017,490(2):98-103. [25]Carlsson AC,Calamia M,Risérus U,et al.Kidney injury molecule (KIM)-1 is associated with insulin resistance: results from two community-based studies of elderly individuals[J].Diabetes Res Clin Pract,2014,103(3):516-521. [26]Kumari M,Sharma R,Pandey G,et al.Deletion of insulin receptor in the proximal tubule and fasting augment albumin excretion[J].J Cell Biochem,2019,120(6):10688-10696. [27]Zhang Y,Yang S,Cui X,et al.Hyperinsulinemia Can Cause Kidney Disease in the IGT Stage of OLETF Rats via the INS/IRS-1/PI3-K/Akt Signaling Pathway[J].J Diabetes Res,2019(2019):4709715. [28]Nizar JM,Shepard BD,Vo VT,et al.Renal tubule insulin receptor modestly promotes elevated blood pressure and markedly stimulates glucose reabsorption[J].JCI Insight,2018,3(16):e95107. [29]Nakamura M,Yamazaki O,Shirai A, et al.Preserved Na/HCO3 cotransporter sensitivity to insulin may promote hypertension in metabolic syndrome[J].Kidney Int,2015,87(3):535-542. [30]Zheng Y,Yamada H,Sakamoto K,et al.Roles of insulin receptor substrates in insulin-induced stimulation of renal proximal bicarbonate absorption[J].J Am Soc Nephrol,2005,16(8):2288-2295. [31]Tanaka M.Improving obesity and blood pressure[J].Hypertens Res,2020,43(2):79-89. [32]Pandey G,Makhija E,George N,et al.Insulin regulates nitric oxide production in the kidney collecting duct cells[J].J Biol Chem,2015,290(9):5582-5591. [33]Asplin JR.Uric acid stones[J].Semin Nephrol,1996,16(5):412-424. [34]Spatola L,Angelini C,Badalamenti S,et al.Kidney stones diseases and glycaemic statuses: focus on the latest clinical evidences[J].Urolithiasis,2017,45(5):457-460. [35]Ichida K.[Hyperuricemia and metabolic syndrome][J].Nihon Yakurigaku Zasshi,2010,136(6):321-324. [36]于艳,何丽洁,王汉民.NLRP1炎性体促进高糖高胰岛素诱导的肾小球系膜细胞焦亡[J].细胞与分子免疫学杂志,2018,34(5):442-447. [37]Subathra M,Korrapati M,Howell LA,et al.Kidney glycosphingolipids are elevated early in diabetic nephropathy and mediate hypertrophy of mesangial cells[J].Am J Physiol Renal Physiol,2015,309(3):F204-F215. [38]Xu WW,Guan MP,Zheng ZJ,et al.Exendin-4 alleviates high glucose-induced rat mesangial cell dysfunction through the AMPK pathway[J].Cell Physiol Biochem,2014,33(2):423-432. [39]Horita S,Nakamura M,Suzuki M,et al.Selective Insulin Resistance in the Kidney[J].Biomed Res Int,2016(2016):5825170. [40]Mima A,Ohshiro Y,Kitada M,et al.Glomerular-specific protein kinase C-β-induced insulin receptor substrate-1 dysfunction and insulin resistance in rat models of diabetes and obesity[J].Kidney Int,2011,79(8):883-896. [41]Sarafidis PA,Lasaridis AN.Insulin Resistance and Endothelin: Another Pathway for Renal Injury in Patients With the Cardiometabolic Syndrome?[J].Journal of the Cardio Metabolic Syndrome,2008,3(3):183-187.

相似文献/References:

[1]吕 宁,徐 昕,黄 永,等.公安民警皮肤软纤维瘤与代谢综合征危险因素相关性研究[J].医学信息,2018,31(10):69.[doi:10.3969/j.issn.1006-1959.2018.10.021]
 LV Ning,XU Xin,HUANG Yong,et al.Correlative Study on Skin Soft Fibroma and Risk Factors of Metabolic Syndrome in Public Security Police[J].Medical Information,2018,31(24):69.[doi:10.3969/j.issn.1006-1959.2018.10.021]
[2]杨锦龙,刘 欢,吕秋菊,等.非糖尿病患者糖化血红蛋白和胰岛素抵抗与 冠状动脉病变程度的相关性研究[J].医学信息,2018,31(10):93.[doi:10.3969/j.issn.1006-1959.2018.10.028]
 YANG Jin-long,LIU Huan,LV Qiu-ju,et al.Correlation between Glycosylated Hemoglobin and Insulin Resistance and Severity of Coronary Artery Disease in Non-diabetic Patients[J].Medical Information,2018,31(24):93.[doi:10.3969/j.issn.1006-1959.2018.10.028]
[3]王清华,易守芳,余明芳.肾移植术后药源性肾损伤生物标志物的研究[J].医学信息,2019,32(10):44.[doi:10.3969/j.issn.1006-1959.2019.10.016]
 WANG Qing-hua,YI Shou-fang,YU Ming-fang.Study on Biomarkers of Drug-induced Renal Injury after Renal Transplantation[J].Medical Information,2019,32(24):44.[doi:10.3969/j.issn.1006-1959.2019.10.016]
[4]谢小莉,李 燕,霍 敏,等.老年2型糖尿病患者轻度认知功能障碍与胰岛素抵抗、 白介素-6的相关性研究[J].医学信息,2019,32(15):97.[doi:10.3969/j.issn.1006-1959.2019.15.030]
 XIE Xiao-li,LI Yan,HUO Min,et al.Correlation between Mild Cognitive Impairment and Insulin Resistance and Interleukin-6 in Elderly Type 2 Diabetic Patients[J].Medical Information,2019,32(24):97.[doi:10.3969/j.issn.1006-1959.2019.15.030]
[5]刘柏基,熊波波.代谢综合征与良性前列腺增生合并下尿路症状的关系 及治疗研究[J].医学信息,2019,32(17):28.[doi:10.3969/j.issn.1006-1959.2019.17.010]
 LIU Bai-ji,XIONG Bo-bo.Relationship between Metabolic Syndrome and Benign Prostatic Hyperplasia with Lower Urinary Tract Symptoms and Treatment[J].Medical Information,2019,32(24):28.[doi:10.3969/j.issn.1006-1959.2019.17.010]
[6]赵 猛,孙 娟,褚 璇.苯扎贝特改善2型糖尿病合并高甘油三酯血症患者 胰岛素抵抗的临床分析[J].医学信息,2019,32(17):145.[doi:10.3969/j.issn.1006-1959.2019.17.048]
 ZHAO Meng,SUN Juan,CHU Xuan.Clinical Analysis of Bezafibrate in Improving Insulin Resistance in Patients with Type 2 Diabetes Mellitus Complicated with Hypertriglyceridemia[J].Medical Information,2019,32(24):145.[doi:10.3969/j.issn.1006-1959.2019.17.048]
[7]李淑娟,王爱芹,杨学军,等.子宫内膜息肉发病相关危险因素临床分析[J].医学信息,2019,32(13):119.[doi:10.3969/j.issn.1006-1959.2019.13.035]
 LI Shu-juan,WANG Ai-qin,YANG Xue-jun,et al.Clinical Analysis of Risk Factors Related to the Incidence of Endometrial Polyps[J].Medical Information,2019,32(24):119.[doi:10.3969/j.issn.1006-1959.2019.13.035]
[8]陈 月,任 伟.胰岛素抵抗与肌少症关系的研究[J].医学信息,2019,32(23):42.[doi:10.3969/j.issn.1006-1959.2019.23.011]
 CHEN Yue,REN Wei.Study on the Relationship Between Insulin Resistance and Sarcopenia[J].Medical Information,2019,32(24):42.[doi:10.3969/j.issn.1006-1959.2019.23.011]
[9]李 玲,宋光耀.健康体检者胰岛素抵抗与血脂异常的相关性及血脂最佳分界值的探讨[J].医学信息,2020,33(01):94.[doi:10.3969/j.issn.1006-1959.2020.01.028]
 LI Ling,SONG Guang-yao.Correlation Between Insulin Resistance and Dyslipidemia and the Best Cut-off Value of Blood Lipids in Healthy People[J].Medical Information,2020,33(24):94.[doi:10.3969/j.issn.1006-1959.2020.01.028]
[10]张晴晴,张瑞霞.Irisin的生理效应及其循环水平的影响因素[J].医学信息,2020,33(02):36.[doi:10.3969/j.issn.1006-1959.2020.02.010]
 ZHANG Qing-qing,ZHANG Rui-xia.The Physiological Effect of Irisin and the Influencing Factors of its Circulation Level[J].Medical Information,2020,33(24):36.[doi:10.3969/j.issn.1006-1959.2020.02.010]

更新日期/Last Update: 1900-01-01