Volume 2 Issue 4
Oct.  2022
Turn off MathJax
Article Contents
Yongting Zhao, Xiaofang Zhang, Haihai Liang, Lihong Wang. Antidiabetic agents: Do they hit the right targets?[J]. Frigid Zone Medicine, 2022, 2(4): 225-243. doi: 10.2478/fzm-2022-0030
Citation: Yongting Zhao, Xiaofang Zhang, Haihai Liang, Lihong Wang. Antidiabetic agents: Do they hit the right targets?[J]. Frigid Zone Medicine, 2022, 2(4): 225-243. doi: 10.2478/fzm-2022-0030

Antidiabetic agents: Do they hit the right targets?

doi: 10.2478/fzm-2022-0030
More Information
  • Corresponding author: Lihong Wang, E-mail: nd6688@163.com
  • Received Date: 2021-07-09
  • Accepted Date: 2022-04-21
  • Available Online: 2022-10-30
  • Diabetes mellitus (DM) is a progressive metabolic disease characterized by chronic hyperglycemia and caused by different degree of pancreatic islet dysfunction and/or insulin resistance (IR). Long course DM can lead to a variety of macrovascular and microvascular complications which involve artery vessels, heart, kidney, retina, nervous system, etc. In recent years, DM has attracted more and more attention due to its high morbidity and mortality. In addition to achieve effective glycemic control, prevention of complications has also been considered a priority for type 2 diabetes mellitus (T2DM) management. Herein, we provide a comprehensive overview on the pharmacotherapeutics for T2DM and perspectives on the future directions of basic and translational research on anti-diabetic therapy and pharmatheutical development of new drugs.

     

  • Conflicts of interests
    All authors declare no competing interests.
  • loading
  • [1]
    Benito-Vicente A, Jebari S, Larrea-Sebal A, et al. Pathophysiology of type 2 diabetes mellitus. Int J Mol Sci, 2020; 21(17): 6275. doi: 10.3390/ijms21176275
    [2]
    Chatterjee S, Khunti K, Davies M J. Type 2 diabetes. Lancet, 2017; 389(10085): 2239-2251. doi: 10.1016/S0140-6736(17)30058-2
    [3]
    Stumvoll M, Goldstein B J, van Haeften T W. Type 2 diabetes: principles of pathogenesis and therapy. Lancet, 2005; 365(9467): 1333-1346. doi: 10.1016/S0140-6736(05)61032-X
    [4]
    Yoon K H, Lee J H, Kim J W, et al. Epidemic obesity and type 2 diabetes in Asia. Lancet, 2006; 368(9548): 1681-1688. doi: 10.1016/S0140-6736(06)69703-1
    [5]
    Weyer C, Bogardus C, Mott D M, et al. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest, 1999; 104(6): 787-794. doi: 10.1172/JCI7231
    [6]
    Christensen A A, Gannon M. The beta cell in type 2 diabetes. Curr Diab Rep, 2019; 19(9): 81. doi: 10.1007/s11892-019-1196-4
    [7]
    Halban P A, Polonsky K S, Bowden D W, et al. Beta-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment. Diabetes Care, 37(6): 1751-1758.
    [8]
    Czech M P. Insulin action and resistance in obesity and type 2 diabetes. Nat Med, 2017; 23(7): 804-814. doi: 10.1038/nm.4350
    [9]
    Pearson T, Wattis J A, King J R, et al. The effects of insulin resistance on individual tissues: an application of a mathematical model of metabolism in humans. Bull Math Biol, 2016; 78(6): 1189-1217. doi: 10.1007/s11538-016-0181-1
    [10]
    Wilcox G. Insulin and insulin resistance. Clin Biochem Rev, 2005; 26(2): 19-39.
    [11]
    Cerf M E. Beta cell dysfunction and insulin resistance. Front Endocrinol (Lausanne), 2013; 4: 37.
    [12]
    Zheng Y, Ley S H, Hu F B. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat Rev Endocrinol, 2018; 14(2): 88-98. doi: 10.1038/nrendo.2017.151
    [13]
    Battisti W P, Palmisano J, Keane W E. Dyslipidemia in patients with type 2 diabetes. relationships between lipids, kidney disease and cardiovascular disease. Clin Chem Lab Med, 2003; 41(9): 1174-1181.
    [14]
    Verges B. Pathophysiology of diabetic dyslipidaemia: where are we? Diabetologia, 2015; 58(5): 886-899. doi: 10.1007/s00125-015-3525-8
    [15]
    Taskinen M R. Diabetic dyslipidaemia: from basic research to clinical practice. Diabetologia, 2003; 46(6): 733-749. doi: 10.1007/s00125-003-1111-y
    [16]
    Chapman M J. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J, 2011; 32(11): 1345-1361. doi: 10.1093/eurheartj/ehr112
    [17]
    Nordestgaard B G, Varbo A. Triglycerides and cardiovascular disease. Lancet, 2014; 384(9943): 626-635. doi: 10.1016/S0140-6736(14)61177-6
    [18]
    Yamamoto W R. Endoplasmic reticulum stress alters ryanodine receptor function in the murine pancreatic beta cell. J Biol Chem, 2019; 294(1): 168-181. doi: 10.1074/jbc.RA118.005683
    [19]
    Lynch S V, Pedersen O. The human intestinal microbiome in health and disease. N Engl J Med, 2016; 375(24): 2369-2379. doi: 10.1056/NEJMra1600266
    [20]
    Li X, Watanabe K, Kimura I. Gut microbiota dysbiosis drives and implies novel therapeutic strategies for diabetes mellitus and related metabolic diseases. Front Immunol, 2017; 8: 1882. doi: 10.3389/fimmu.2017.01882
    [21]
    Tang C, Ahmed K, Gille A, et al. Loss of FFA2 and FFA3 increases insulin secretion and improves glucose tolerance in type 2 diabetes. Nat Med, 2015; 21(2): 173-177. doi: 10.1038/nm.3779
    [22]
    Petersen K F, Befroy D, Dufour S, et al. Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Science, 2003; 300(5622): 1140-1142. doi: 10.1126/science.1082889
    [23]
    Kim J A, Wei Y, Sowers J R. Role of mitochondrial dysfunction in insulin resistance. Circ Res, 2008; 102(4): 401-414. doi: 10.1161/CIRCRESAHA.107.165472
    [24]
    Schofield J H, Schafer Z T. Mitochondrial reactive oxygen species and mitophagy: a complex and nuanced relationship. Antioxid Redox Signal, 2021; 34(7): 517-530. doi: 10.1089/ars.2020.8058
    [25]
    Kadowaki T, Kadowaki H, Mori Y, et al. A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA. N Engl J Med, 1994; 330(14): 962-968. doi: 10.1056/NEJM199404073301403
    [26]
    Tawata M, Hayashi J I, Isobe K, et al. A new mitochondrial DNA mutation at 14577 T/C is probably a major pathogenic mutation for maternally inherited type 2 diabetes. Diabetes, 2000; 49(7): 1269-1272. doi: 10.2337/diabetes.49.7.1269
    [27]
    Wang D, Taniyama M, Suzuki Y, et al. Association of the mitochondrial DNA 5178A/C polymorphism with maternal inheritance and onset of type 2 diabetes in Japanese patients. Exp Clin Endocrinol Diabetes, 2001; 109(7): 361-364.
    [28]
    Nesto R W. Correlation between cardiovascular disease and diabetes mellitus: current concepts. Am J Med, 2004; 116(Suppl 5A): 11S-22S.
    [29]
    Haffner S M, Lehto S, Ronnemaa T, et al. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med, 1998; 339(4): 229-234. doi: 10.1056/NEJM199807233390404
    [30]
    Beckman J A, Creager M A, Libby P. Diabetes and atherosclerosis: epidemiology, pathophysiology, and management. JAMA, 2002; 287(19): 2570-2581. doi: 10.1001/jama.287.19.2570
    [31]
    Holman R R, Paul S K, Bethel M A, et al. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med, 2008; 359(15): 1577-1589. doi: 10.1056/NEJMoa0806470
    [32]
    Turner R C, Cull C A, Frighi V, et al. Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies (UKPDS 49). UK Prospective Diabetes Study (UKPDS) Group. JAMA, 1999; 281(21): 2005-2012.
    [33]
    Ihnat M A, Thorpe J E, Kamat C D, et al. Reactive oxygen species mediate a cellular 'memory' of high glucose stress signalling. Diabetologia, 2007; 50(7): 1523-1531. doi: 10.1007/s00125-007-0684-2
    [34]
    Olsen A S, Sarras Jr M P, Leontovich A, et al. Heritable transmission of diabetic metabolic memory in zebrafish correlates with DNA hypomethylation and aberrant gene expression. Diabetes, 2012; 61(2): 485-491. doi: 10.2337/db11-0588
    [35]
    Poy M N, Hausser J, Trajkovski M, et al. miR-375 maintains normal pancreatic alpha-and beta-cell mass. Proc Natl Acad Sci U S A, 2009; 106(14): 5813-5818. doi: 10.1073/pnas.0810550106
    [36]
    Reddy M A, Zhang E, Natarajan R. Epigenetic mechanisms in diabetic complications and metabolic memory. Diabetologia, 2015; 58(3): 443-455. doi: 10.1007/s00125-014-3462-y
    [37]
    Brasacchio D, Okabe J, Tikellis C, et al. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes, 2009; 58(5): 1229-1236. doi: 10.2337/db08-1666
    [38]
    Al-Haddad R, Karnib N, Assaad R A, et al. Epigenetic changes in diabetes. Neurosci Lett, 2016; 625: 64-69. doi: 10.1016/j.neulet.2016.04.046
    [39]
    Ceriello A, Ihnat M A, Thorpe J E. Clinical review 2: The "metabolic memory": is more than just tight glucose control necessary to prevent diabetic complications? J Clin Endocrinol Metab, 2009; 94(2): 410-415. doi: 10.1210/jc.2008-1824
    [40]
    Nishikawa T, Edelstein D, Du X L, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature, 2000; 404(6779): 787-790. doi: 10.1038/35008121
    [41]
    Reddy M A, Natarajan R. Epigenetic mechanisms in diabetic vascular complications. Cardiovasc Res, 2011; 90(3): 421-429. doi: 10.1093/cvr/cvr024
    [42]
    Guarner V, Rubio-Ruiz M E. Low-grade systemic inflammation connects aging, metabolic syndrome and cardiovascular disease. Interdiscip Top Gerontol, 2015; 40: 99-106.
    [43]
    Flory J, Lipska K. Metformin in 2019. JAMA, 2019; 322(13): 1926-1927.
    [44]
    American Diabetes Association. 9. Pharmacologic approaches to glycemic treatment: standards of medical care in diabetes-2019. Diabetes Care, 2019; 42(Supl 1): S90-S102.
    [45]
    Turner R C, Holman R R, Stratton I M. Effect of intensive bloodglucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet, 1998; 352(9131): 854-865. doi: 10.1016/S0140-6736(98)07037-8
    [46]
    De Vries S T, Denig P, Ekhart C, et al. Sex differences in adverse drug reactions of metformin: a longitudinal survey study. Drug Saf, 2020; 43(5): 489-495. doi: 10.1007/s40264-020-00913-8
    [47]
    Rena G, Hardie D G, Pearson E R. The mechanisms of action of metformin. Diabetologia, 2017; 60(9): 1577-1585. doi: 10.1007/s00125-017-4342-z
    [48]
    Knowler W C, Barrett-Connor E, Fowle S E, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med, 2002; 346(6): 393-403. doi: 10.1056/NEJMoa012512
    [49]
    Markowicz-Piasecka M, Sikora J, Szydlowska A, et al. Metformin-a future therapy for neurodegenerative diseases: theme: drug discovery, development and delivery in alzheimer's disease guest editor: davide brambilla. Pharm Res, 2017; 34(12): 2614-2627. doi: 10.1007/s11095-017-2199-y
    [50]
    Hundal R S, Inzucchi S E. Metformin: new understandings, new uses. Drugs, 2003; 63(18): 1879-1894. doi: 10.2165/00003495-200363180-00001
    [51]
    Martin-Montalvo A, Mercken E M, Mitchell S J, et al. Metformin improves healthspan and lifespan in mice. Nat Commun, 2013; 4: 2192. doi: 10.1038/ncomms3192
    [52]
    Pearce E L, Walsh M C, Cejas P J, et al. Enhancing CD8 T-cell memory by modulating fatty acid metabolism. Nature, 2009; 460(7251): 103-107. doi: 10.1038/nature08097
    [53]
    Sui X, Xu Y, Wang X, et al. Metformin: a novel but controversial drug in cancer prevention and treatment. Mol Pharm, 2015; 12(11): 3783-3791. doi: 10.1021/acs.molpharmaceut.5b00577
    [54]
    Podhorecka M, Ibanez B, Dmoszynska A. Metformin-its potential anti-cancer and anti-aging effects. Postepy Hig Med Dosw (Online), 2017; 71: 170-175.
    [55]
    McCreight L J, Bailey C J, Pearson E R. Metformin and the gastrointestinal tract. Diabetologia, 2016; 59(3): 426-435. doi: 10.1007/s00125-015-3844-9
    [56]
    Shaw R J, Lamia K A, Vasquez D, et al. The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. Science, 2005; 310(5754): 1642-1646. doi: 10.1126/science.1120781
    [57]
    Singh A K, Gupta R, Ghosh A, et al. Diabetes in COVID-19: Prevalence, pathophysiology, prognosis and practical considerations. Diabetes Metab Syndr, 2020; 14(4): 303-310. doi: 10.1016/j.dsx.2020.04.004
    [58]
    Pal R, Bhadada S K. COVID-19 and diabetes mellitus: An unholy interaction of two pandemics. Diabetes Metab Syndr, 2020; 14(4): 513-517. doi: 10.1016/j.dsx.2020.04.049
    [59]
    Bornstein S R, Rubino F, Khunti K, et al. Practical recommendations for the management of diabetes in patients with COVID-19. Lancet Diabetes Endocrinol, 2020; 8(6): 546-550. doi: 10.1016/S2213-8587(20)30152-2
    [60]
    Scheen A J. Metformin and COVID-19: From cellular mechanisms to reduced mortality. Diabetes Metab, 2020; 46(6): 423-426. doi: 10.1016/j.diabet.2020.07.006
    [61]
    Huang I, Lim M A, Pranata, R. Diabetes mellitus is associated with increased mortality and severity of disease in COVID-19 pneumonia-A systematic review, meta-analysis, and meta-regression. Diabetes Metab Syndr, 2020; 14(4): 395-403. doi: 10.1016/j.dsx.2020.04.018
    [62]
    Bramante C T, Ingraham N E, Murray T A, et al. Observational Study of Metformin and Risk of Mortality in Patients Hospitalized with Covid-19. Lancet Healthy Longev, 2021; 2(1): e34-e41. doi: 10.1016/S2666-7568(20)30033-7
    [63]
    Sola D, Rossi L, Schianca G P C, et al. Sulfonylureas and their use in clinical practice. Arch Med Sci, 2015; 11(4): 840-848.
    [64]
    Melander A, Lebovitz H E, Faber O K. Sulfonylureas. Why, which, and how? Diabetes Care, 1990; 13(Suppl 3): 18-25.
    [65]
    Marshall A, Gingerich R L, Wright P H. Hepatic effect of sulfonylureas. Metabolism, 1970; 19(12): 1046-1052. doi: 10.1016/0026-0495(70)90028-4
    [66]
    Landstedt-Hallin L, Adamson U, Lins P E. Oral glibenclamide suppresses glucagon secretion during insulin-induced hypoglycemia in patients with type 2 diabetes. J Clin Endocrinol Metab, 1999; 84(9): 3140-3145.
    [67]
    Scarsi M, Podvinec M, Roth A, et al. Sulfonylureas and glinides exhibit peroxisome proliferator-activated receptor gamma activity: a combined virtual screening and biological assay approach. Mol Pharmacol, 2007; 71(2): 398-406. doi: 10.1124/mol.106.024596
    [68]
    Müller G. Dynamics of plasma membrane microdomains and crosstalk to the insulin signalling cascade. FEBS Lett, 2002; 531(1): 1-87. doi: 10.1016/S0014-5793(02)03452-X
    [69]
    Nakano N, Miyazawa N, Sakurai T, et al. Gliclazide inhibits proliferation but stimulates differentiation of white and brown adipocytes. J Biochem, 2007; 142(5): 639-645. doi: 10.1093/jb/mvm172
    [70]
    Sena C M, Louro T, Matafome P, et al. Antioxidant and vascular effects of gliclazide in type 2 diabetic rats fed high-fat diet. Physiol Res, 2009; 58(2): 203-209.
    [71]
    Lee K Y, Kim J R, Choi H C. Gliclazide, a KATP channel blocker, inhibits vascular smooth muscle cell proliferation through the CaMKKbeta-AMPK pathway. Vascul Pharmacol, 2018; 102: 21-28. doi: 10.1016/j.vph.2018.01.001
    [72]
    Rados D V, Pinto L C, Remonti L R, et al. Correction: The association between sulfonylurea use and all-cause and cardiovascular mortality: a meta-analysis with trial sequential analysis of randomized clinical trials. PLoS Med, 13(6): e1002091 doi: 10.1371/journal.pmed.1002091
    [73]
    Sehra D, Sehra S. Hypertension in type 2 diabetes mellitus: do we need to redefine the role of sulfonylureas? Recent Adv Cardiovasc Drug Discov, 2015; 10(1): 4-9.
    [74]
    Webb D R, Davies M J, Jarvis J, et al. The right place for Sulphonylureas today. Diabetes Res Clin Pract, 2019; 157: 107836. doi: 10.1016/j.diabres.2019.107836
    [75]
    Thisted H, Johnsen S P, Rungby J. Sulfonylureas and the risk of myocardial infarction. Metabolism, 2006; 55(5 Suppl 1): S16-S19.
    [76]
    Ramracheya R, Ward C, Shigeto M, et al. Membrane potentialdependent inactivation of voltage-gated ion channels in alpha-cells inhibits glucagon secretion from human islets. Diabetes, 2010; 59(9): 2198-2208. doi: 10.2337/db09-1505
    [77]
    Braun M, Ramracheya R, Amisten S, et al. Somatostatin release, electrical activity, membrane currents and exocytosis in human pancreatic delta cells. Diabetologia, 2009; 52(8): 1566-1578. doi: 10.1007/s00125-009-1382-z
    [78]
    Blumenthal S A. Potentiation of the hepatic action of insulin by chlorpropamide. Diabetes, 1977; 26(5): 485-489. doi: 10.2337/diab.26.5.485
    [79]
    Lv W, Wang X, Xu Q, et al. Mechanisms and characteristics of sulfonylureas and glinides. Curr Top Med Chem, 2020; 20(1): 37-56. doi: 10.2174/1568026620666191224141617
    [80]
    Ballmann M, Hubert D, Assael B M, et al. Repaglinide versus insulin for newly diagnosed diabetes in patients with cystic fibrosis: a multicentre, open-label, randomised trial. Lancet Diabetes Endocrinol, 2018; 6(2): 114-121. doi: 10.1016/S2213-8587(17)30400-X
    [81]
    Fuhlendorff J, Rorsman P, Kofod H, et al. Stimulation of insulin release by repaglinide and glibenclamide involves both common and distinct processes. Diabetes, 1998; 47(3): 345-351. doi: 10.2337/diabetes.47.3.345
    [82]
    Davies M J. Insulin secretagogues. Curr Med Res Opin, 2002; 18(Suppl 1): s22-s30.
    [83]
    Zhou X Y, Zhu J, Bao Z J, et al. A variation in KCNQ1 gene is associated with repaglinide efficacy on insulin resistance in Chinese Type 2 Diabetes Mellitus Patients. Sci Rep, 2016; 6: 37293. doi: 10.1038/srep37293
    [84]
    Xiao Z X, Chen R Q, Hu D X, et al. Identification of repaglinide as a therapeutic drug for glioblastoma multiforme. Biochem Biophys Res Commun, 2017; 488(1): 33-39. doi: 10.1016/j.bbrc.2017.04.157
    [85]
    Ford E S. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: a summary of the evidence. Diabetes Care, 2005; 28(7): 1769-1778. doi: 10.2337/diacare.28.7.1769
    [86]
    Buchanan T A, Xiang A H, Peters R K, et al. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Diabetes, 2002; 51(9): 2796-2803. doi: 10.2337/diabetes.51.9.2796
    [87]
    Diamant M, Heine R J. Thiazolidinediones in type 2 diabetes mellitus: current clinical evidence. Drugs, 2003; 63(13): 1373-1405. doi: 10.2165/00003495-200363130-00004
    [88]
    Reusch J E, Regensteiner J G, Watson P A. Novel actions of thiazolidinediones on vascular function and exercise capacity. Am J Med, 2003; 115(Suppl 8A): 69S-74S.
    [89]
    Giles T D, Sander G E. Effects of thiazolidinediones on blood pressure. Curr Hypertens Rep, 2007; 9(4): 332-337. doi: 10.1007/s11906-007-0060-0
    [90]
    Ko G J, Kang Y S, Han S Y, et al. Pioglitazone attenuates diabetic nephropathy through an anti-inflammatory mechanism in type 2 diabetic rats. Nephrol Dial Transplant, 2008; 23(9): 2750-2760. doi: 10.1093/ndt/gfn157
    [91]
    Sarafidis P A, Grekas D M. Insulin resistance and oxidant stress: an interrelation with deleterious renal consequences? J Cardiometab Syndr, 2007; 2(2): 39-142.
    [92]
    Pistrosch F, Herbrig K, Kindel B, et al. Rosiglitazone improves glomerular hyperfiltration, renal endothelial dysfunction, and microalbuminuria of incipient diabetic nephropathy in patients. Diabetes, 2005; 54(7): 2206-2211. doi: 10.2337/diabetes.54.7.2206
    [93]
    Sarafidis P A, Bakris G L. Protection of the kidney by thiazolidinediones: an assessment from bench to bedside. Kidney Int, 2006; 70(7): 1223-1233. doi: 10.1038/sj.ki.5001620
    [94]
    Buckingham R E, Al-barazanji K A, Toseland C D, et al. Peroxisome proliferator-activated receptor-gamma agonist, rosiglitazone, protects against nephropathy and pancreatic islet abnormalities in Zucker fatty rats. Diabetes, 1998; 47(8): 1326-1334.
    [95]
    Yoshimoto T, Naruse M, Nishikawa M, et al. Antihypertensive and vasculo-and renoprotective effects of pioglitazone in genetically obese diabetic rats. Am J Physiol, 1997; 272(6 Pt 1): E989-E996.
    [96]
    Nesto R W, Bell D, Bonow R O, et al. Thiazolidinedione use, fluid retention, and congestive heart failure: a consensus statement from the American Heart Association and American Diabetes Association. Diabetes Care, 2004; 27(1): 256-263. doi: 10.2337/diacare.27.1.256
    [97]
    Sarafidis P A, Stafylas P C, Georgianos P I, et al. Effect of thiazolidinediones on albuminuria and proteinuria in diabetes: a metaanalysis. Am J Kidney Dis, 2010; 55(5): 835-847. doi: 10.1053/j.ajkd.2009.1
    [98]
    Tseng Y H, Tsan Y T, Chan W C, et al. Use of an alpha-glucosidase inhibitor and the risk of colorectal cancer in patients with diabetes: a nationwide, population-based cohort study. Diabetes Care, 2015; 38(11): 2068-2074. doi: 10.2337/dc15-0563
    [99]
    Tamez-Perez H E, Proskauer-Pena S L, Hernrndez-Coria M I, et al. AACE comprehensive diabetes management algorithm 2013. Endocrine practice. Endocr Pract, 2013; 19(4): 736-737. doi: 10.4158/EP13210.LT
    [100]
    Van de Laa F A, Kucassen P L B, Akkermans R P, et al. Alphaglucosidase inhibitors for type 2 diabetes mellitus. Cochrane Database Syst Rev, 2005; 2005(2): CD003639.
    [101]
    Standl E, Schnell O, McGuire D K. Heart failure considerations of antihyperglycemic medications for type 2 diabetes. Circ Res, 2016; 118(11): 1830-1843. doi: 10.1161/CIRCRESAHA.116.306924
    [102]
    Hoffmann J, Spengler M. Efficacy of 24-week monotherapy with acarbose, glibenclamide, or placebo in NIDDM patients. The Essen Study. Diabetes Care, 1994; 17(6): 561-566. doi: 10.2337/diacare.17.6.561
    [103]
    Chiasson J L. Acarbose for the prevention of diabetes, hypertension, and cardiovascular disease in subjects with impaired glucose tolerance: the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) Trial. Endocr Pract, 2006; 12(Suppl 1): 25-30.
    [104]
    Han X, Deng Y P, Yu J W, et al. Acarbose accelerates wound healing via Akt/eNOS signaling in db/db Mice. Oxid Med Cell Longev, 2017; 2017: 7809581.
    [105]
    Dodds S G, Parihar M, Javors M, et al. Acarbose improved survival for Apc(+/Min) mice. Aging Cell, 2020; 19(2): e13088.
    [106]
    Smith B J, Miller R A, Ericsson A C, et al. Changes in the gut microbiome and fermentation products concurrent with enhanced longevity in acarbose-treated mice. BMC Microbiol, 2019; 19(1): 130. doi: 10.1186/s12866-019-1494-7
    [107]
    Kang S H, Jung D J, Choi E W, et al. Association between lowgrade albuminuria and hearing impairment in a non-diabetic Korean population: The Korea National Health and Nutrition Examination Survey (2011-2013). Ann Med, 2015; 47(8): 664-672. doi: 10.3109/07853890.2015.1093163
    [108]
    Chida S, Fujita Y, Ogawa A, et al. Levels of albuminuria and risk of developing macroalbuminuria in type 2 diabetes: historical cohort study. Sci Rep, 2016; 6: 26380. doi: 10.1038/srep26380
    [109]
    Pan Q, Xu Y, Yang N, et al. Metformin or acarbose treatment significantly reduced albuminuria in patients with newly diagnosed type 2 diabetes mellitus and low-grade albuminuria. Med Sci Monit, 2018; 24: 8941-8949. doi: 10.12659/MSM.911979
    [110]
    Chen X, Zheng Y, Shen Y. Voglibose (Basen, AO-128), one of the most important alpha-glucosidase inhibitors. Curr Med Chem, 2006; 13(1): 109-116. doi: 10.2174/092986706789803035
    [111]
    Scott L J, Spencer C M. Miglitol: a review of its therapeutic potential in type 2 diabetes mellitus. Drugs, 2000; 59(3): 521-549. doi: 10.2165/00003495-200059030-00012
    [112]
    Wang H, Shen Y, Zhao L, et al. 1-Deoxynojirimycin and its derivatives: a mini review of the literature. Curr Med Chem, 2021; 28(3): 628-643. doi: 10.2174/0929867327666200114112728
    [113]
    Wang N, Minatoguchi S, Chen X H, et al. Antidiabetic drug miglitol inhibits myocardial apoptosis involving decreased hydroxyl radical production and Bax expression in an ischaemia/reperfusion rabbit heart. Br J Pharmacol, 2004; 142(6): 983-990. doi: 10.1038/sj.bjp.0705863
    [114]
    Tan K, Tesar C, Wilton R, et al. Interaction of antidiabetic alphaglucosidase inhibitors and gut bacteria alpha-glucosidase. Protein Sci, 2018; 27(8): 1498-1508. doi: 10.1002/pro.3444
    [115]
    Kojima Y, Kimura T, Nakagawa K, et al. Effects of mulberry leaf extract rich in 1-deoxynojirimycin on blood lipid profiles in humans. J Clin Biochem Nutr, 2010; 47(2): 155-161. doi: 10.3164/jcbn.10-53
    [116]
    Silva C H, Taft C A. Computer-aided molecular design of novel glucosidase inhibitors for AIDS treatment. J Biomol Struct Dyn, 2004; 22(1): 59-63. doi: 10.1080/07391102.2004.10506981
    [117]
    Wang R J, Yang C H, Hu M L. 1-Deoxynojirimycin inhibits metastasis of B16F10 melanoma cells by attenuating the activity and expression of matrix metalloproteinases-2 and -9 and altering cell surface glycosylation. J Agric Food Chem, 2010; 58(16): 8988-8993. doi: 10.1021/jf101401b
    [118]
    American Diabetes Association. Standards of medical care in diabetes——2012. Diabetes Care 35(Suppl 1): S11-S63.
    [119]
    Capuano A, Sportiello L, Maiorino M I, et al. Dipeptidyl peptidase-4 inhibitors in type 2 diabetes therapy——focus on alogliptin. Drug Des Devel Ther, 2013; 7: 989-1001.
    [120]
    Rizzo M R, Barbieri M, Marfella R, et al. Response to comment on: Rizzo et al. Reduction of oxidative stress and inflammation by blunting daily acute glucose fluctuations in patients with type 2 diabetes: role of dipeptidyl peptidase-Ⅳ inhibition. Diabetes Care, 2012; 35: 2076-2082.
    [121]
    Lee S, Lee H, Kim Y, et al. Effect of DPP-Ⅳ inhibitors on glycemic variability in patients with T2DM: a systematic review and meta-analysis. Sci Rep, 2019; 9(1): 13296. doi: 10.1038/s41598-019-49803-9
    [122]
    Drucker D J, Nauck M A. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet, 2006; 368(9548): 1696-1705. doi: 10.1016/S0140-6736(06)69705-5
    [123]
    Drucker D J. The biology of incretin hormones. Cell Metab, 2006; 3(3): 153-165. doi: 10.1016/j.cmet.2006.01.004
    [124]
    Inaba W, Mizukami H, Kamata K, et al. Effects of long-term treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin on islet endocrine cells in non-obese type 2 diabetic Goto-Kakizaki rats. Eur J Pharmacol, 2012; 691(1-3): 297-306. doi: 10.1016/j.ejphar.2012.07.030
    [125]
    Kröller-Schön S, Knorr M, Hausding M, et al. Glucose-independent improvement of vascular dysfunction in experimental sepsis by dipeptidyl-peptidase 4 inhibition. Cardiovasc Res, 2012; 96(1): 140-149. doi: 10.1093/cvr/cvs246
    [126]
    Ye Y M, Keyes K T, Zhang C F, et al. The myocardial infarct sizelimiting effect of sitagliptin is PKA-dependent, whereas the protective effect of pioglitazone is partially dependent on PKA. Am J Physiol Heart Circ Physiol, 2010; 298(5): H1454-H1465. doi: 10.1152/ajpheart.00867.2009
    [127]
    Read P A, Khan F Z, Heck P M, et al. DPP-4 inhibition by sitagliptin improves the myocardial response to dobutamine stress and mitigates stunning in a pilot study of patients with coronary artery disease. Circ Cardiovasc Imaging, 2010; 3(2): 195-201.
    [128]
    Yilmaz Y, Atug O, Yonal O, et al. Dipeptidyl peptidase Ⅳ inhibitors: therapeutic potential in nonalcoholic fatty liver disease. Med Sci Monit 2009; 15(4): HY1-5.
    [129]
    Liao X Y, Song L Y, Zeng B H, et al. Alteration of gut microbiota induced by DPP-4i treatment improves glucose homeostasis. EBioMedicine, 2019; 44: 665-674. doi: 10.1016/j.ebiom.2019.03.057
    [130]
    Shah Z, Kampfrath T, Deiuliis J A, et al. Long-term dipeptidylpeptidase 4 inhibition reduces atherosclerosis and inflammation via effects on monocyte recruitment and chemotaxis. Circulation, 2011; 124(21): 2338-2349. doi: 10.1161/CIRCULATIONAHA.111.041418
    [131]
    Salaga M, Binienda A, Draczkowski P, et al. Novel peptide inhibitor of dipeptidyl peptidase Ⅳ (Tyr-Pro-D-Ala-NH2) with anti-inflammatory activity in the mouse models of colitis. Peptides, 2018; 108: 34-45. doi: 10.1016/j.peptides.2018.08.011
    [132]
    Zhang X W, Zhang Z W, Li M Z, et al. Potential role of dipeptidyl peptidase-4 inhibitors in atrial fibrillation. Int J Cardiol, 2016; 207: 46-47.
    [133]
    Green J B, Bethel M A, Armstrong P W, et al. Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes. N Engl J Med, 2015; 373(3): 232-242. doi: 10.1056/NEJMoa1501352
    [134]
    Rosenstock J, Perkovic V, Johansen O E, et al. Effect of linagliptin vs placebo on major cardiovascular events in adults with type 2 diabetes and high cardiovascular and renal risk: the CARMELINA randomized clinical trial. JAMA, 2019; 321(1): 69-79. doi: 10.1001/jama.2018.18269
    [135]
    Mascolo A, Rafaniello C, Sportiello L, et al. Dipeptidyl peptidase (DPP)-4 inhibitor-induced arthritis/arthralgia: a review of clinical cases. Drug Saf, 2016; 39(5): 401-407. doi: 10.1007/s40264-016-0399-8
    [136]
    De S, Banerjee S, Kumar S K A, et al. Critical role of dipeptidyl peptidase Ⅳ: a therapeutic target for diabetes and cancer. Mini Rev Med Chem, 2019; 19(2): 88-97.
    [137]
    Amritha C A, Kumaravelu P, Chellathai D D. Evaluation of anti cancer effects of DPP-4 inhibitors in colon cancer-an invitro study. J Clin Diagn Res, 2015; 9(12): FC14-16.
    [138]
    Pandey J, Tamrakar A K. SGLT2 inhibitors for the treatment of diabetes: a patent review (2013-2018). Expert Opin Ther Pat, 2019; 29(5): 369-384. doi: 10.1080/13543776.2019.1612879
    [139]
    Min S H, Yoon J H, Hahn S, et al. Comparison between SGLT2 inhibitors and DPP4 inhibitors added to insulin therapy in type 2 diabetes: a systematic review with indirect comparison meta-analysis. Diabetes Metab Res Rev, 2017; 33(1): 27155214.
    [140]
    Sonne D P, Hemmingsen B. Comment on American diabetes association. Standards of medical care in diabetes-2017. Diabetes Care, 2017; 40(Suppl. 1): S1-S135. .
    [141]
    Verma S, McMurray J J V. SGLT2 inhibitors and mechanisms of cardiovascular benefit: a state-of-the-art review. Diabetologia, 2018; 61(10): 2108-2117. doi: 10.1007/s00125-018-4670-7
    [142]
    Mangoni A A, Mircoli L, Giannattasio C, et al. Effect of sympathectomy on mechanical properties of common carotid and femoral arteries. Hypertension, 1997; 30(5): 1085-1088. doi: 10.1161/01.HYP.30.5.1085
    [143]
    Hijmering M L, Stroes E S G, Olijhoek J, et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol, 2002; 39(4): 683-688. doi: 10.1016/S0735-1097(01)01786-7
    [144]
    DiBona G F. Sympathetic nervous system and the kidney in hypertension. Curr Opin Nephrol Hypertens, 2002; 11(2): 197-200. doi: 10.1097/00041552-200203000-00011
    [145]
    Lytvyn Y, Bjornstad P, Udell J A, et al. Sodium glucose cotransporter-2 inhibition in heart failure: potential mechanisms, clinical applications, and summary of clinical trials. Circulation, 2017; 136(17): 1643-1658. doi: 10.1161/CIRCULATIONAHA.117.030012
    [146]
    Han J H, Oh T J, Lee G, et al. The beneficial effects of empagliflozin, an SGLT2 inhibitor, on atherosclerosis in ApoE (-/-) mice fed a western diet. Diabetologia, 2017; 60(2): 364-376. doi: 10.1007/s00125-016-4158-2
    [147]
    Zelniker T A, Braunwald E. Cardiac and renal effects of sodiumglucose co-transporter 2 inhibitors in diabetes: JACC state-of-the-art review. J Am Coll Cardiol, 2018; 72(15): 1845-1855. doi: 10.1016/j.jacc.2018.06.040
    [148]
    Liu B, Wang Y, Zhang Y, et al. Mechanisms of protective effects of SGLT2 inhibitors in cardiovascular disease and renal dysfunction. Curr Top Med Chem, 2019; 19(20): 1818-1849. doi: 10.2174/1568026619666190828161409
    [149]
    Maejima Y. SGLT2 inhibitors play a salutary role in heart failure via modulation of the mitochondrial function. Front Cardiovasc Med, 2019; 6: 186.
    [150]
    Ishibashi Y, Matsui T, Yamagishi S. Tofogliflozin, a highly selective inhibitor of SGLT2 blocks proinflammatory and proapoptotic effects of glucose overload on proximal tubular cells partly by suppressing oxidative stress generation. Horm Metab Res, 2016; 48(3): 191-195.
    [151]
    Zinman B, Wanner C, Lachin J M, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med, 2015; 373(22): 2117-2128. doi: 10.1056/NEJMoa1504720
    [152]
    Kawanami D, Matoba K, Takeda Y, et al. SGLT2 Inhibitors as a therapeutic option for diabetic nephropathy. Int J Mol Sci, 2017; 18(5): 1083. doi: 10.3390/ijms18051083
    [153]
    Terami N, Ogawa D, Tachibana H, et al. Long-term treatment with the sodium glucose cotransporter 2 inhibitor, dapagliflozin, ameliorates glucose homeostasis and diabetic nephropathy in db/db mice. PLoS One 9, 2014; 9(6): e100777. doi: 10.1371/journal.pone.0100777
    [154]
    Lee Y H, Kim S H, Kang J M, et al. Empagliflozin attenuates diabetic tubulopathy by improving mitochondrial fragmentation and autophagy. Am J Physiol Renal Physiol, 2019; 317(4): F767-F780. doi: 10.1152/ajprenal.00565.2018
    [155]
    Wang X X, Levi J, Lu Y H, et al. SGLT2 protein expression is increased in human diabetic nephropathy: SGLT2 protein inhibition decreases renal lipid accumulation, inflammation, and the development of nephropathy in diabetic mice. J Biol Chem, 2017; 292(13): 5335-5348. doi: 10.1074/jbc.M117.779520
    [156]
    Shibuya T, Fushimi N, Kawai M, et al. Luseogliflozin improves liver fat deposition compared to metformin in type 2 diabetes patients with non-alcoholic fatty liver disease: A prospective randomized controlled pilot study. Diabetes Obes Metab, 2018; 20(2): 438-442. doi: 10.1111/dom.13061
    [157]
    Leiter L A, Forst T, Polidori D, et al. Effect of canagliflozin on liver function tests in patients with type 2 diabetes. Diabetes Metab, 2016; 42(1): 25-32. doi: 10.1016/j.diabet.2015.10.003
    [158]
    Komiya C, Tsuchiya K, Shiba K, et al. Ipragliflozin improves hepatic steatosis in obese mice and liver dysfunction in type 2 diabetic patients irrespective of body weight reduction. PLoS One, 2016; 11(3): e0151511. doi: 10.1371/journal.pone.0151511
    [159]
    Prattichizzo F, Nigris V D, Spiga R, et al. Inflammageing and metaflammation: The Yin and Yang of type 2 diabetes. Ageing Res Rev, 2018; 41: 1-17. doi: 10.1016/j.arr.2017.10.003
    [160]
    Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol, 2012; 32(9): 2045-2051. doi: 10.1161/ATVBAHA.108.179705
    [161]
    Karasawa T, Takahashi M. Role of NLRP3 inflammasomes in atherosclerosis. J Atheroscler Thromb, 2017; 24(5): 443-451. doi: 10.5551/jat.RV17001
    [162]
    Garvey W T, Van Gaal L, Leiter L A, et al. Effects of canagliflozin versus glimepiride on adipokines and inflammatory biomarkers in type 2 diabetes. Metabolism, 2018; 85: 32-37. doi: 10.1016/j.metabol.2018.02.002
    [163]
    Xu L, Ota T. Emerging roles of SGLT2 inhibitors in obesity and insulin resistance: Focus on fat browning and macrophage polarization. Adipocyte, 2018; 7(2): 121-128.
    [164]
    Packer M. Do sodium-glucose co-transporter-2 inhibitors prevent heart failure with a preserved ejection fraction by counterbalancing the effects of leptin? A novel hypothesis. Diabetes Obes Metab, 2018; 20(6): 1361-1366. doi: 10.1111/dom.13229
    [165]
    Diaz-Rodríguez E, Agra R M, Fernández Á L, et al. Effects of dapagliflozin on human epicardial adipose tissue: modulation of insulin resistance, inflammatory chemokine production, and differentiation ability. Cardiovasc Res, 2018; 114(2): 336-346. doi: 10.1093/cvr/cvx186
    [166]
    Ye Y, Bajaj M, Yang H C, et al. SGLT-2 Inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Further augmentation of the effects with saxagliptin, a DPP4 inhibitor. Cardiovasc Drugs Ther, 2017; 31(2): 119-132. doi: 10.1007/s10557-017-6725-2
    [167]
    Lee T M, Chang N C, Lin S Z. Dapagliflozin, a selective SGLT2 Inhibitor, attenuated cardiac fibrosis by regulating the macrophage polarization via STAT3 signaling in infarcted rat hearts. Free Radic Biol Med, 2017; 104: 298-310. doi: 10.1016/j.freeradbiomed.2017.01.035
    [168]
    Naznin F, Sakoda H, Okada T, et al. Canagliflozin, a sodium glucose cotransporter 2 inhibitor, attenuates obesity-induced inflammation in the nodose ganglion, hypothalamus, and skeletal muscle of mice. Eur J Pharmacol, 2017; 794: 37-44. doi: 10.1016/j.ejphar.2016.11.028
    [169]
    Komatsu S, Nomiyama T, Numata T, et al. SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation. Endocr J, 2020; 67(1): 99-106. doi: 10.1507/endocrj.EJ19-0428
    [170]
    Guo M, Ding J Y, Li J S, et al. SGLT2 inhibitors and risk of stroke in patients with type 2 diabetes: A systematic review and meta-analysis. Diabetes Obes Metab, 2018; 20(8): 1977-1982. doi: 10.1111/dom.13295
    [171]
    Tentolouris A, Vlachakis P, Tzeravini E, et al. SGLT2 inhibitors: a review of their antidiabetic and cardioprotective effects. Int J Environ Res Public Health, 2019; 16(16): 2965. doi: 10.3390/ijerph16162965
    [172]
    Yabe D, Nishikino R, Kaneko M, et al. Short-term impacts of sodium/glucose co-transporter 2 inhibitors in Japanese clinical practice: considerations for their appropriate use to avoid serious adverse events. Expert Opin Drug Saf, 2015; 14(6): 795-800. doi: 10.1517/14740338.2015.1034105
    [173]
    Lee Y S, Jun H S. Anti-inflammatory effects of GLP-1-based therapies beyond glucose control. Mediators Inflamm, 2016; 2016: 3094642.
    [174]
    Inzucchi S E, Bergenstal R M, Buse J B, et al. Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach: update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care, 2015; 38(1): 140-149. doi: 10.2337/dc14-2441
    [175]
    Drucker D J. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metab, 2018; 27(4): 740-756. doi: 10.1016/j.cmet.2018.03.001
    [176]
    Gentilella R, Pechtner V, Corcos A, et al. Glucagon-like peptide-1 receptor agonists in type 2 diabetes treatment: are they all the same? Diabetes Metab Res Rev, 2019; 35(1): e3070. doi: 10.1002/dmrr.3070
    [177]
    Arden C. A role for Glucagon-like peptide-1 in the regulation of beta-cell autophagy. Peptides, 2018; 100: 85-93. doi: 10.1016/j.peptides.2017.12.002
    [178]
    Zummo F P, Cullen K S, Honkanen-Scott M, et al. Glucagonlike peptide 1 protects pancreatic beta-cells from death by increasing autophagic flux and restoring lysosomal function. Diabetes, 2017; 66(5): 1272-1285. doi: 10.2337/db16-1009
    [179]
    Lim S W, Jin L, Jin J, et al. Effect of exendin-4 on autophagy clearance in beta cell of rats with tacrolimus-induced diabetes mellitus. Sci Rep, 2016; 6: 29921. doi: 10.1038/srep29921
    [180]
    Dokken B B, La Bonte L R, Davis-Gorman G, et al. Glucagon-like peptide-1 (GLP-1), immediately prior to reperfusion, decreases neutrophil activation and reduces myocardial infarct size in rodents. Horm Metab Res, 2011; 43(5): 300-305. doi: 10.1055/s-0031-1271777
    [181]
    Tate M, Robinson E, Green B D, et al. Exendin-4 attenuates adverse cardiac remodelling in streptozocin-induced diabetes via specific actions on infiltrating macrophages. Basic Res Cardiol, 2016; 111(1): 1. doi: 10.1007/s00395-015-0518-1
    [182]
    Gaspari T, Brdar M, Lee H W, et al. Molecular and cellular mechanisms of glucagon-like peptide-1 receptor agonist-mediated attenuation of cardiac fibrosis. Diab Vasc Dis Res, 2016; 13(1): 56-68. doi: 10.1177/1479164115605000
    [183]
    Heppner K M, Perez-Tilve D. GLP-1 based therapeutics: simultaneously combating T2DM and obesity. Front Neurosci, 2015; 9: 92.
    [184]
    Perry T, Lahiri D K, Sambamurti K, et al. Glucagon-like peptide-1 decreases endogenous amyloid-beta peptide (Abeta) levels and protects hippocampal neurons from death induced by abeta and iron. J Neurosci Res, 2003; 72(5): 603-612. doi: 10.1002/jnr.10611
    [185]
    de Graaf C, Donnelly D, Wootten D, et al. Glucagon-like peptide-1 and its class B G protein-coupled receptors: a long march to therapeutic successes. Pharmacol Rev, 2016; 68(4): 954-1013. doi: 10.1124/pr.115.011395
    [186]
    Kodera R, Shikata K, Kataoka H U, et al. Glucagon-like peptide-1 receptor agonist ameliorates renal injury through its anti-inflammatory action without lowering blood glucose level in a rat model of type 1 diabetes. Diabetologia, 2011; 54(4): 965-978. doi: 10.1007/s00125-010-2028-x
    [187]
    Hsieh J, Longuet C, Baker C L, et al. The glucagon-like peptide 1 receptor is essential for postprandial lipoprotein synthesis and secretion in hamsters and mice. Diabetologia, 2010; 53(3): 552-561. doi: 10.1007/s00125-009-1611-5
    [188]
    Xiao C, Bandsma R H, Dash S, et al. Exenatide, a glucagonlike peptide-1 receptor agonist, acutely inhibits intestinal lipoprotein production in healthy humans. Arterioscler Thromb Vasc Biol, 2012; 32(6): 1513-1519. doi: 10.1161/ATVBAHA.112.246207
    [189]
    Armstrong M J, Gaunt P, Aithal G P, et al. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, randomised, placebo-controlled phase 2 study. Lancet, 2016; 387(10019): 679-690. doi: 10.1016/S0140-6736(15)00803-X
    [190]
    Gou S, Zhu T, Wang W, et al. Glucagon like peptide-1 attenuates bleomycin-induced pulmonary fibrosis, involving the inactivation of NFkappaB in mice. Int Immunopharmacol, 2014; 22(2): 498-504. doi: 10.1016/j.intimp.2014.07.010
    [191]
    Faillie J L, Yu O H, Yin H, et al. Association of bile duct and gallbladder diseases with the use of incretin-based drugs in patients with type 2 diabetes mellitus. JAMA Intern Med, 2016; 176(10): 1474-1481. doi: 10.1001/jamainternmed.2016.1531
    [192]
    Holman R R, Bethel M A, Mentz R J, et al. Effects of once-weekly exenatide on cardiovascular outcomes in type 2 diabetes. N Engl J Med, 2017; 377(13): 1228-1239. doi: 10.1056/NEJMoa1612917
    [193]
    Marso S P, Daniels G H, Brown-Frandsen K, et al. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med, 2016; 375(4): 311-322. doi: 10.1056/NEJMoa1603827
    [194]
    Fullerton B, Siebenhofer A, Jeitler K, et al. Short-acting insulin analogues versus regular human insulin for adult, non-pregnant persons with type 2 diabetes mellitus. Cochrane Database Syst Rev, 2018; 12(12): CD013228.
    [195]
    Semlitsch T, Engler J, Siebenhofer A, et al. (Ultra-)long-acting insulin analogues versus NPH insulin (human isophane insulin) for adults with type 2 diabetes mellitus. Cochrane Database Syst Rev, 2020; 11(11): CD005613.
    [196]
    Kruger D F, Novak L M. Role of ultrafast-acting insulin analogues in the management of diabetes. J Am Assoc Nurse Pract, 2019; 31(9): 537-548. doi: 10.1097/JXX.0000000000000261
    [197]
    Hussain H, Green I R, Abbas G, et al. Protein tyrosine phosphatase 1B (PTP1B) inhibitors as potential anti-diabetes agents: patent review (2015-2018). Expert Opin Ther Pat, 2019; 29(9): 689-702. doi: 10.1080/13543776.2019.1655542
    [198]
    Eleftheriou P, Geronikaki A, Petrou A. PTP1b inhibition, a promising approach for the treatment of diabetes type Ⅱ. Curr Top Med Chem, 2019; 19(4): 246-263. doi: 10.2174/1568026619666190201152153
    [199]
    Tamrakar A K, Maurya C K, Rai A K. PTP1B inhibitors for type 2 diabetes treatment: a patent review (2011-2014). Expert Opin Ther Pat, 2014; 24(10): 1101-1115. doi: 10.1517/13543776.2014.947268
    [200]
    Wang L J, Jiang B, Wu N, et al. Small molecules as potent protein tyrosine phosphatase 1B (PTP1B) inhibitors documented in patents from 2009 to 2013. Mini Rev Med Chem, 2015; 15: 104-122 doi: 10.2174/1389557515666150203144339
    [201]
    Verma M, Gupta S J, Chaudhary A, et al. Protein tyrosine phosphatase 1B inhibitors as antidiabetic agents-A brief review. Bioorg Chem, 2016; 70: 267-283.
    [202]
    Johnson T O, Ermolieff J, Jirousek M R. Protein tyrosine phosphatase 1B inhibitors for diabetes. Nat Rev Drug Discov, 2002; 1(9): 696-709. doi: 10.1038/nrd895
    [203]
    Duarte A M, Guarino M P, Barroso S, et al. Phytopharmacological strategies in the management of type 2 diabetes mellitus. Foods, 2020; 9(3): 271. doi: 10.3390/foods9030271
    [204]
    Grewal A S, Bhardwaj S, Pandita D, et al. Updates on aldose reductase inhibitors for management of diabetic complications and nondiabetic diseases. Mini Rev Med Chem, 2016; 16(2): 120-162.
    [205]
    Quattrini L, La Motta C. Aldose reductase inhibitors: 2013-present. Expert Opin Ther Pat, 2009; 29(3): 199-213.
    [206]
    Kawanishi K, Ueda H, Moriyasu M. Aldose reductase inhibitors from the nature. Curr Med Chem, 2003; 10(15): 1353-1374. doi: 10.2174/0929867033457304
    [207]
    Oka M, Kato N. Aldose reductase inhibitors. J Enzyme Inhib, 2001; 16(6): 465-473. doi: 10.1080/14756360127568
    [208]
    Ramunno A, Cosconati S, Sartini S, et al. Progresses in the pursuit of aldose reductase inhibitors: the structure-based lead optimization step. Eur J Med Chem, 2012; 51: 216-226. doi: 10.1016/j.ejmech.2012.02.045
    [209]
    Jedziniak J A, Kinoshita J H. Activators and inhibitors of lens aldose reductase. Invest Ophthalmol, 1971; 10(5): 357-366.
    [210]
    Kousaxidis A, Petrou A, Lavrentaki V, et al. Aldose reductase and protein tyrosine phosphatase 1B inhibitors as a promising therapeutic approach for diabetes mellitus. Eur J Med Chem, 2020; 207: 112742. doi: 10.1016/j.ejmech.2020.112742
    [211]
    Persaud S J. Islet G-protein coupled receptors: therapeutic potential for diabetes. Curr Opin Pharmacol, 2017; 37: 24-28. doi: 10.1016/j.coph.2017.08.001
    [212]
    Riddy D M, Delerive P, Summers R J, et al. G Protein-Coupled Receptors Targeting Insulin Resistance, Obesity, and Type 2 Diabetes Mellitus. Pharmacol Rev 2018; 70(1): 39-67. doi: 10.1124/pr.117.014373
    [213]
    Sebastiani G, Ceccarelli E, Castagna M G, et al. G-protein-coupled receptors (GPCRs) in the treatment of diabetes: Current view and future perspectives. Best Pract Res Clin Endocrinol Metab, 2018; 32(2): 201-213. doi: 10.1016/j.beem.2018.02.005
    [214]
    Hoque M, Ali S, Hoda M. Current status of G-protein coupled receptors as potential targets against type 2 diabetes mellitus. Int J Biol Macromol, 2018; 118(Pt 8): 2237-2244.
    [215]
    Reimann F, Gribble F M. G protein-coupled receptors as new therapeutic targets for type 2 diabetes. Diabetologia, 2006; 59(2): 229-233.
    [216]
    Ritter K, Buning C, Halland N, et al. G Protein-Coupled Receptor 119 (GPR119) agonists for the treatment of diabetes: recent progress and prevailing challenges. J Med Chem, 2016; 59(8): 3579-3592. doi: 10.1021/acs.jmedchem.5b01198
    [217]
    Mancini A D, Poitout V. GPR40 agonists for the treatment of type 2 diabetes: life after 'TAKing' a hit. Diabetes Obes Metab, 2015; 17(7): 622-629. doi: 10.1111/dom.12442
    [218]
    Katz L B, Gambale J J, Rothenberg P L, et al. Effects of JNJ-38431055, a novel GPR119 receptor agonist, in randomized, doubleblind, placebo-controlled studies in subjects with type 2 diabetes. Diabetes Obes Metab, 2012; 14(8): 709-716. doi: 10.1111/j.1463-1326.2012.01587.x
    [219]
    Kim Y, Keogh J B, Clifton P M. Polyphenols and glycemic control. Nutrients, 2016; 8(1): 17. doi: 10.3390/nu8010017
    [220]
    Hung H Y, Qian K, Morris-Natschke S L, et al. Recent discovery of plant-derived anti-diabetic natural products. Nat Prod Rep, 2012; 29(5): 580-606. doi: 10.1039/c2np00074a
    [221]
    Öztürk E, Arslan A K K, Yerer M B, et al. Resveratrol and diabetes: A critical review of clinical studies. Biomed Pharmacother, 2017; 95: 230-234. doi: 10.1016/j.biopha.2017.08.070
    [222]
    Szkudelski T, Szkudelska K. Resveratrol and diabetes: from animal to human studies. Biochim Biophys Acta, 2015; 1852(6): 1145-1154. doi: 10.1016/j.bbadis.2014.10.013
    [223]
    Timmers S, de Ligt M, Phielix E, et al. Resveratrol as add-on therapy in subjects with well-controlled type 2 diabetes: a randomized controlled trial. Diabetes Care, 2016; 39(12): 2211-2217. doi: 10.2337/dc16-0499
    [224]
    Jeyaraman M M, Al-Yousif N S H, Singh Mann A, et al. Resveratrol for adults with type 2 diabetes mellitus. Cochrane Database Syst Rev, 2020; 1(1): CD011919.
    [225]
    Pivari F, Mingione A, Brasacchio C, et al. Curcumin and type 2 diabetes mellitus: prevention and treatment. Nutrients, 2019; 11(8): 1837. doi: 10.3390/nu11081837
    [226]
    Nabavi S F, Thiagarajan R, Rastrelli L, et al. Curcumin: a natural product for diabetes and its complications. Curr Top Med Chem, 2015; 15(23): 2445-2455. doi: 10.2174/1568026615666150619142519
    [227]
    Chuengsamarn S, Rattanamongkolgul S, Luechapudiporn R, et al. Curcumin extract for prevention of type 2 diabetes. Diabetes Care, 2012; 35(11): 2121-2127. doi: 10.2337/dc12-0116
    [228]
    Neerati P, Devde R, Gangi A K. Evaluation of the effect of curcumin capsules on glyburide therapy in patients with type-2 diabetes mellitus. Phytother Res, 2014; 28(12): 1796-1800. doi: 10.1002/ptr.5201
    [229]
    Yin J, Xing H, Ye J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism, 2008; 57(5): 712-717. doi: 10.1016/j.metabol.2008.01.013
    [230]
    Lan J, Zhao Y Y, Dong F X, et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. J Ethnopharmacol, 2015; 161: 69-81. doi: 10.1016/j.jep.2014.09.049
    [231]
    Liang Y, Xu X J, Yin M J, et al. Effects of berberine on blood glucose in patients with type 2 diabetes mellitus: a systematic literature review and a meta-analysis. Endocr J, 2019; 66(1): 51-63.
    [232]
    Zhang H, Wei J, Xue R, et al. Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Metabolism, 2010; 59(2): 285-292. doi: 10.1016/j.metabol.2009.07.029
    [233]
    Emerging Risk Factors Collaboration, Di Angelantonio E, Kaptoge S, et al. Association of Cardiometabolic Multimorbidity With Mortality. JAMA, 2015; 314(1): 52-60. doi: 10.1001/jama.2015.7008
    [234]
    Dinesh Shah A, Langenberg C, Rapsomaniki E, et al. Type 2 diabetes and incidence of a wide range of cardiovascular diseases: a cohort study in 1.9 million people. Lancet, 2015; 385(Suppl 1): S86.
    [235]
    Mannino G C, Andreozzi F, Sesti G. Pharmacogenetics of type 2 diabetes mellitus, the route toward tailored medicine. Diabetes Metab Res Rev, 2019; 35(3): e3109. doi: 10.1002/dmrr.3109
    [236]
    Eng C, Kramer C K, Zinman B, et al. Glucagon-like peptide-1 receptor agonist and basal insulin combination treatment for the management of type 2 diabetes: a systematic review and meta-analysis. Lancet, 2014; 384(9961): 2228-2234. doi: 10.1016/S0140-6736(14)61335-0
    [237]
    Gao H, Xiao J N, Sun Q, et al. A single decoy oligodeoxynucleotides targeting multiple oncoproteins produces strong anticancer effects. Mol Pharmacol, 2006; 70(5): 1621-1629. doi: 10.1124/mol.106.024273
    [238]
    Lu Y, Xiao J N, Lin H X, et al. A single anti-microRNA antisense oligodeoxyribonucleotide (AMO) targeting multiple microRNAs offers an improved approach for microRNA interference. Nucleic Acids Res, 2009; 37(3): e24. doi: 10.1093/nar/gkn1053
    [239]
    Wang Z G. The concept of multiple-target anti-miRNA antisense oligonucleotide technology. Methods Mol Biol, 2011; 676: 51-57.
    [240]
    Roth B L, Sheffler D J, Kroeze W K. Magic shotguns versus magic bullets: selectively non-selective drugs for mood disorders and schizophrenia. Nat Rev Drug Discov, 2004; 3(4): 353-359. doi: 10.1038/nrd1346
    [241]
    Koutsouleris N, Meisenzahl EM, Borgwardt S, et al. Individualized differential diagnosis of schizophrenia and mood disorders using neuroanatomical biomarkers. Brain, 2015; 138(Pt 7): 2059-2073.
    [242]
    Schwartz S S, Epstein S, Corkey B E, et al. The time is right for a new classification system for diabetes: rationale and implications of the betacell-centric classification schema. Diabetes Care, 2016; 39(2): 179-186. doi: 10.2337/dc15-1585
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(1)  / Tables(2)

    Article Metrics

    Article views (70) PDF downloads(3) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return