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基于“代谢记忆”的糖尿病并发症发生机制及其治疗药物研究进展

汤茜, 陈松, 高向东

汤茜, 陈松, 高向东. 基于“代谢记忆”的糖尿病并发症发生机制及其治疗药物研究进展[J]. 中国药科大学学报, 2017, 48(5): 622-628. DOI: 10.11665/j.issn.1000-5048.20170519
引用本文: 汤茜, 陈松, 高向东. 基于“代谢记忆”的糖尿病并发症发生机制及其治疗药物研究进展[J]. 中国药科大学学报, 2017, 48(5): 622-628. DOI: 10.11665/j.issn.1000-5048.20170519
TANG Qian, CHEN Song, GAO Xiangdong. Advances of mechanisms of metabolic memory-based diabetic complications and therapeutic drugs[J]. Journal of China Pharmaceutical University, 2017, 48(5): 622-628. DOI: 10.11665/j.issn.1000-5048.20170519
Citation: TANG Qian, CHEN Song, GAO Xiangdong. Advances of mechanisms of metabolic memory-based diabetic complications and therapeutic drugs[J]. Journal of China Pharmaceutical University, 2017, 48(5): 622-628. DOI: 10.11665/j.issn.1000-5048.20170519

基于“代谢记忆”的糖尿病并发症发生机制及其治疗药物研究进展

基金项目: 国家自然科学基金资助项目(No.81473216,No.81673435)

Advances of mechanisms of metabolic memory-based diabetic complications and therapeutic drugs

  • 摘要: 代谢记忆是有效管理糖尿病并发症的主要障碍,仅通过药物控制血糖水平并不能同时防治糖尿病相关的多种并发症发生。因此,了解其介导糖尿病并发症发生的分子机制,有助于对预防和消除“代谢记忆”效应进行更深入的研究。本文将对受代谢记忆影响的相关糖尿病并发症、代谢记忆介导糖尿病并发症发生的分子机制以及预期的治疗药物进行综述,为防治代谢记忆的进一步研究提供依据。
    Abstract: At present, metabolic memory is a major obstacle hindering the effective control of diabetes. Controlling blood sugar level solely by drugs can not prevent multiple diabetic complications. Understanding the molecular mechanisms of mediating diabetic complications, therefore, will eliminate the “metabolic memory” effect. In this artical, the molecular mechanism of metabolic memory mediating diabetic complications and prospective treatment drugs were reviewed, which provides basis to the further research on prevention and treatment of metabolic memory.
  • [1] Berezin A.Metabolic memory phenomenon in diabetes mellitus:achieving and perspectives[J].Diabetes Metab Syndr,2016,10(2 Suppl 1):S176-S183.
    [2] de Oliveira AA,de Oliveira TF,Bobadilla LL,et al.Sustained kidney biochemical derangement in treated experimental diabetes:a clue to metabolic memory[J].Sci Rep,2017,7:40544.
    [3] Maghbooli Z,Hossein-nezhad A,Larijani B,et al.Global DNA methylation as a possible biomarker for diabetic retinopathy[J].Diabetes Metab Res Rev,2015,31(2):183-189.
    [4] Motiejūnaite R,Kazlauskas A.Pericytes and ocular diseases[J].Exp Eye Res,2008,86(2):171-177.
    [5] Cho SJ,Roman G,Yeboah F,et al.The road to advanced glycation end products:a mechanistic perspective[J].Curr Med Chem,2007,14(15):1653-1671.
    [6] Pop-Busui R,Martin C.Neuropathy in the DCCT/EDIC-what was done then and what we would do better now[J].Int Rev Neurobiol,2016,127:9-25.
    [7] Javed S,Alam U,Malik RA.Burning through the pain:treatments for diabetic neuropathy[J].Diabetes Obes Metab,2015,17(12):1115-1125.
    [8] Tesfaye S, Boulton AJ, Dyck PJ, et al. Diabetic neuropathies:update on definitions,diagnostic criteria,estimation of severity,and treatments[J].Diabetes Care,2010,33(10):2285-2293.
    [9] Bahniwal M,Little JP,Klegeris A.High glucose enhances neurotoxicity and inflammatory cytokine secretion by stimulated human astrocytes[J].Curr Alzheimer Res,2017,14(7):731-741.
    [10] Chilelli NC,Burlina S,Lapolla A.AGEs,rather than hyperglycemia,are responsible for microvascular complications in diabetes:a “glycoxidation-centric” point of view[J].Nutr Metab Cardiovasc Dis,2013,23(10):913-919.
    [11] Piperi C,Goumenos A,Adamopoulos C,et al.AGE/RAGE signalling regulation by miRNAs:associations with diabetic complications and therapeutic potential[J].Int J Biochem Cell Biol,2015,60:197-201.
    [12] Yamagishi S,Matsui T,Fukami K.Role of receptor for advanced glycation end products(RAGE)and its ligands in cancer risk[J].Rejuvenation Res,2015,18(1):48-56.
    [13] Koulis C,Watson AM,Gray SP,et al.Linking RAGE and Nox in diabetic micro- and macrovascular complications[J].Diabetes Metab,2015,41(4):272-281.
    [14] Yamagishi S,Matsui T.Role of receptor for advanced glycation end products(RAGE)in liver disease[J].Eur J Med Res,2015,20:15.
    [15] Yamagishi S I,Fukami K,Matsui T.Crosstalk between advanced glycation end products(AGEs)-receptor RAGE axis and dipeptidyl peptidase-4-incretin system in diabetic vascular complications[J].Cardiovasc Diabetol,2015,14(1):2.
    [16] Manigrasso MB, Juranek J, Ramasamy R, et al. Unlocking the biology of RAGE in diabetic microvascular complications[J].Trends Endocrinol Metab,2014,25(1):15-22.
    [17] Yamagishi SI,Nakamura N,Matsui T.Glycation and cardiovascular disease in diabetes:a perspective on the concept of metabolic memory[J].J Diabetes,2017,9(2):141-148.
    [18] Voronova V,Zhudenkov K,Helmlinger G,et al.Interpretation of metabolic memory phenomenon using a physiological systems model:what drives oxidative stress following glucose normalization[J]?PLoS ONE,2017,12(2):e0171781.
    [19] Ceriello A,Ihnat MA,Thorpe JE.Clinical review 2:The “metabolic memory”:is more than just tight glucose control necessary to prevent diabetic complications[J]?J Clin Endocrinol Metab,2009,94(2):410-415.
    [20] Zhao S,Li T,Li J,et al.miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway[J].Diabetologia,2016,59(3):644-654.
    [21] Infante-Garcia C,Ramos-Rodriguez JJ,Galindo-Gonzalez L,et al.Long-term central pathology and cognitive impairment are exacerbated in a mixed model of Alzheimer′s disease and type 2 diabetes[J].Psychoneuroendocrinology,2016,65:15-25.
    [22] Chentli F,Azzoug S,Mahgoun S.Diabetes mellitus in elderly[J].Indian J Endocrinol Metab,2015,19(6):744-752.
    [23] Martins FO,Delgado TC,Viegas J,et al.Mechanisms by which the thiazolidinedione troglitazone protects against sucrose-induced hepatic fat accumulation and hyperinsulinaemia[J].Br J Pharmacol,2016,173(2):267-278.
    [24] Nathan DM.Diabetes:advances in diagnosis and treatment[J].JAMA,2015,314(10):1052-1062.
    [25] Yoshida T,Yamagishi S,Nakamura K,et al.Telmisartan inhibits AGE-induced C-reactive protein production through downregulation of the receptor for AGE via peroxisome proliferator-activated receptor-gamma activation[J].Diabetologia,2006,49(12):3094-3099.
    [26] Katz PM,Leiter LA.The role of the kidney and SGLT2 inhibitors in type 2 diabetes[J].Can J Diabetes,2015,39(Suppl 5):S167-S175.
    [27] Shimo N,Matsuoka TA,Miyatsuka T,et al.Short-term selective alleviation of glucotoxicity and lipotoxicity ameliorates the suppressed expression of key β-cell factors under diabetic conditions[J].Biochem Biophys Res Commun,2015,467(4):948-954.
    [28] Dai Y, Dai D, Wang X, et al. DPP-4 inhibitors repress NLRP3 inflammasome and interleukin-1beta via GLP-1 receptor in macrophages through protein kinase C pathway[J].Cardiovasc Drugs Ther,2014,28(5):425-432.
    [29] Broxmeyer HE,Pelus LM.Inhibition of DPP4/CD26 and dmPGE2 treatment enhances engraftment of mouse bone marrow hematopoietic stem cells[J].Blood Cells Mol Dis,2014,53(1/2):34-38.
    [30] Zheng Z,Chen H,Li J,et al.Sirtuin 1-mediated cellular metabolic memory of high glucose via the LKB1/AMPK/ROS pathway and therapeutic effects of metformin[J].Diabetes,2012,61(1):217-228.
    [31] Hanefeld M,Monnier L,Schnell O,et al.Early treatment with basal insulin glargine in people with type 2 diabetes: lessons from ORIGIN and other cardiovascular trials[J].Diabetes Ther,2016,7(2):187-201.
    [32] Ma L,Lu N,Wu G.Antiplatelet aggregation and endothelial protection of I4,a new synthetic anti-diabetes sulfonylurea compound[J].Platelets,2015,26(4):342-348.
    [33] Hemmingsen B,Lund SS,Gluud C,et al.Targeting intensive glycaemic control versus targeting conventional glycaemic control for type 2 diabetes mellitus[J].Cochrane Database Syst Rev,2011(6):CD008143.
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  • 刊出日期:  2017-10-24

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