Advantages of therapy with sodium glucose cotransporter type 2 inhibitors in patients with type 2 diabetes mellitus in combination with hyperuricemia and gout

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Abstract

Currently, only two drugs for reducing uric acid (UA), allopurinol and febuxostat, are registered in the Russian Federation, but their use does not allow to achieve the target level of UA in all cases. According to the results of numerous randomized trials, hyperuricemia and gout are associated with the corresponding components of the metabolic syndrome, including diabetes mellitus. The influence of factors is due to the need to search for new drugs that have a complex effect on several components of metabolic syndrome at once. Potentially attractive in this regard is a new group of drugs for the treatment of type 2 diabetes mellitus – inhibitors of the sodium-glucose cotransporter of type 2, which, in addition to the main hypoglycemic actions, showed positive effects on the cardiovascular system, kidneys, as well as lowering UA.

About the authors

T. S. Panevin

Nasonova Research Institute of Rheumatology; National Medical Research Center for Endocrinology

Author for correspondence.
Email: tarasel@list.ru
ORCID iD: 0000-0002-5290-156X

врач-эндокринолог; врач-ревматолог 

 
Russian Federation, Moscow

M. S. Eliseev

Nasonova Research Institute of Rheumatology

Email: tarasel@list.ru
ORCID iD: 0000-0003-1191-5831

к.м.н., ст. науч. сотр.

Russian Federation, Moscow

M. V. Shestakova

National Medical Research Center for Endocrinology

Email: tarasel@list.ru
ORCID iD: 0000-0002-5057-127X

акад. РАН, дир. Института диабета

Russian Federation, Moscow

E. L. Nasonov

Nasonova Research Institute of Rheumatology

Email: tarasel@list.ru
ORCID iD: 0000-0002-1598-8360

акад. РАН, науч. рук.

Russian Federation, Moscow

References

  1. Насонова В.А., Барскова В.Г. Ранние диагностика и лечение подагры – научно обоснованное требование улучшения трудового и жизненного прогноза больных. Научно-практическая ревматология. 2004;42(1):5-7 [Nasonova VA, Barskova VG. Early diagnostic and treatment of gout – is scientifically based reguirements for improvement of labour and living prognosis of patients. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2004;42(1):5-7 (In Russ.)]. doi: 10.14412/1995-4484-2004-1374
  2. Насонов Е.Л., Елисеев М.С. Роль интерлейкина 1 в развитии заболеваний человека. Научно-практическая ревматология. 2016;54(1):60-77 [Nasonov EL, Eliseev MS. Role of interleukin 1 in the development ofhuman diseases. Nauchno-prakticheskaya revmatologiya = Rheumatology Science and Practice. 2016;54(1):60-77 (In Russ.)]. doi: 10.14412/1995-4484-2016-60-77
  3. Shiozawa A, Szabo SM, Bolzani A, et al. Serum Uric Acid and the Risk of Incident and Recurrent Gout: A Systematic Review. J Rheumatol. 2017;44(3):388-96. doi: 10.3899/jrheum.160452
  4. Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheumatism. 1972;15(2):189-92. doi: 10.1002/art.1780150209
  5. Cicero AFG, Fogacci F, Giovannini M, et al. Serum uric acid predicts incident metabolic syndrome in the elderly in an analysis of the Brisighella Heart Study. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-29955-w
  6. Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26(2):186-91. doi: 10.1097/bor.0000000000000028
  7. Laws A, Reaven GM. Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations. J Int Med. 1992;231(1):25-30. doi: 10.1111/j.1365-2796.1992.tb00494.x
  8. Abbasian M, Ebrahimi H, Delvarianzadeh M, et al. Association between serum uric acid (SUA) levels and metabolic syndrome (MetS) components in personnel of Shahroud University of Medical Sciences. Diabetes & Metabolic Syndrome. Clin Res Rev. 2016;10(3):132-6. doi: 10.1016/j.dsx.2016.01.003
  9. Verdecchia P, Schillaci G, Reboldi G, et al. Relation Between Serum Uric Acid and Risk of Cardiovascular Disease in Essential Hypertension. Hypertension. 2000;36(6):1072-8. doi: 10.1161/01.hyp.36.6.1072
  10. Zuo T, Liu X, Jiang L, et al. Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies. BMC Cardiovasc Dis. 2016;16(1):207. doi: 10.1186/s12872-016-0379-z71
  11. White J, Sofat R, Hemani G, et al. Plasma urate concentration and risk of coronary heart disease: a Mendelian randomisation analysis. Lancet Diabet Endocrinol. 2016;4(4):327-36. doi: 10.1016/S2213-8587(15)00386-1
  12. Hyndman D, Liu S, Miner JN. Urate Handling in the Human Body. Curr Rheumatol Rep. 2016;18:34. doi: 10.1007/s11926-016-0587-7
  13. Richette P, Doherty M, Pascual E, et al. 2018 updated European League Against Rheumatism evidence-based recommendations for the diagnosis of gout. Ann Rheum Dis. 2020;79(Issue 1). doi: 10.1136/annrheumdis-2019-215315
  14. Khanna D, Fitzgerald JD, Khanna PP, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic non pharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res. 2012;64(10):1431-46. doi: 10.1002/acr.21772
  15. Елисеев М.С. Подагра. В кн.: Ревматология. Российские клинические рекомендации. Под ред. Е.Л. Насонова. М.: ГЭОТАР-Медиа, 2017; с. 253-64 [Eliseev MS. Podagra. V kn.: Revmatologiia. Rossiiskie klinicheskie rekomendatsii. Pod red. EL Nasonova. Moscow: GEOTAR-Media, 2017; p. 253-64 (In Russ.)].
  16. Барскова В.Г., Елисеев М.С., Кудаева Ф.М. и др. Влияние метформина на течение подагры и инсулинорезистентность. Клиническая медицина. 2009;87(7):41-6 [Barskova VG, Eliseev MS, Kudaeva FM, et al. Effect of metformine on the clinical course of gout and insulin resistance. Clinical medicine. 2009;87(7):41-6 (In Russ.)].
  17. Niu S-W, Chang K-T, Lin HY-H, et al. Decreased incidence of gout in diabetic patients using pioglitazone. Rheumatology. 2017;57(1):92-9. doi: 10.1093/rheumatology/kex363
  18. Vallon V. The Mechanisms and Therapeutic Potential of SGLT2 Inhibitors in Diabetes Mellitus. Ann Rev Med. 2015;66(1):255-70. doi: 10.1146/annurev-med-051013-110046
  19. Buchanan KD. Diabetes mellitus and gout. Semin Arthritis Rheumatism. 1972;2(2):157-63. doi: 10.1016/0049-0172(72)90007-8
  20. Tung Y-C, Lee S-S, Tsai W-C, et al. Association Between Gout and Incident Type 2 Diabetes Mellitus: A Retrospective Cohort Study. Am J Med. 2016;129(11):1219.e17-1219.e25. doi: 10.1016/j.amjmed.2016.06.041
  21. Collier A, Stirling A, Cameron L, et al. Gout and diabetes: a common combination. Postgrad Med J. 2016;92(1089):372-8. doi: 10.1136/ postgradmedj-2015-133691
  22. Bhole V, Choi JWJ, Woo Kim S, et al. Serum Uric Acid Levels and the Risk of Type 2 Diabetes: A Prospective Study. Am J Med. 2010;123(10):957-61. doi: 10.1016/j.amjmed.2010.03.027
  23. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15. doi: 10.1002/art.22466
  24. Елисеев М.С., Барскова В.Г. Нарушения углеводного обмена при подагре: частота выявления и клинические особенности. Терапевтический архив. 2010;82(5):50-4 [Eliseev MS, Barskova VG. Carbo-hydrate metabolic disturbances in gout: Detection rate and clinical features. Therapeutic Archive. 2010;82(5):50-4 (In Russ.)].
  25. Liu J, Tao L, Zhao Z, et al. Two-Year Changes in Hyperuricemia and Risk of Diabetes: A Five-Year Prospective Cohort Study. J Diabet Res. 2018;2018:1-7. doi: 10.1155/2018/6905720
  26. Choi BG, Kim DJ, Baek MJ, et al. Hyperuricaemia and development of type 2 diabetes mellitus in Asian population. Clin Exper Pharmacol Physiol. 2018;45(6):499-506. doi: 10.1111/1440-1681.12911
  27. Shani M, Vinker S, Dinour D, et al. High Normal Uric Acid Levels Are Associated with an Increased Risk of Diabetes in Lean, Normoglycemic Healthy Women. J Clin Endocrinol Metab. 2016;101(10):3772-8. doi: 10.1210/jc.2016-2107
  28. Li L, Yang C, Zhao Y, et al. Is hyperuricemia an independent risk factor for new-onset chronic kidney disease: a systematic review and meta-analysis based on observational cohort studies. BMC Nephrology. 2014;15(1). doi: 10.1186/1471-2369-15-122
  29. De Cosmo S, Viazzi F, Pacilli A, et al. Serum Uric Acid and Risk of CKD in Type 2 Diabetes. Clin J Am Soc Nephrol. 2015;10(11):1921-9. doi: 10.2215/cjn.03140315
  30. Ito H, Abe M, Mifune M, et al. Hyperuricemia Is Independently Associated with Coronary Heart Disease and Renal Dysfunction in Patients with Type 2 Diabetes Mellitus. Sesti G, editor. PLoS ONE. 2011;6(11):e27817. doi: 10.1371/journal.pone.0027817
  31. Choi Y-J, Yoon Y, Lee K-Y, et al. Uric acid induces endothelial dysfunction by vascular insulin resistance associated with the impairment of nitric oxide synthesis. FASEB J. 2014;28(7):3197-204. doi: 10.1096/fj.13-247148
  32. Fabbrini E, Serafini M, Colic Baric I, et al. Effect of Plasma Uric Acid on Antioxidant Capacity, Oxidative Stress, and Insulin Sensitivity in Obese Subjects. Diabetes. 2013;63(3):976-81. doi: 10.2337/db13-1396
  33. Glantzounis G, Tsimoyiannis E, Kappas A, Galaris D. Uric Acid and Oxidative Stress. Curr Pharm Design. 2005;11(32):4145-51. doi: 10.2174/138161205774913255
  34. Kuwabara M, Niwa K, Hisatome I, et al. Asymptomatic Hyperuricemia Without Comorbidities Predicts Cardiometabolic Diseases. Hypertension. 2017;69(6):1036-44. doi: 10.1161/hypertensionaha.116.08998
  35. Fonseca VA. Defining and Characterizing the Progression of Type 2 Diabetes. Diabetes Care. 2009;32(Suppl. 2):S151-S156. doi: 10.2337/dc09-s301
  36. Li C, Hsieh MC, Chang SJ. Metabolic syndrome, diabetes, and hyperuricemia. Curr Opin Rheumatol. 2013;25(2):210-6. doi: 10.1097/BOR.0b013e32835d951e
  37. Dessein PH. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000;59(7):539-43. doi: 10.1136/ard.59.7.539
  38. Bruderer SG, Bodmer M, Jick SS, Meier CR. Poorly controlled type 2 diabetes mellitus is associated with a decreased risk of incident gout: a population-based case-control study. Ann Rheum Dis. 2014;74(9):1651-8. doi: 10.1136/annrheumdis-2014-205337
  39. Lin S-D, Tsai D-H, Hsu S-R. Association between serum uric acid level and components of the metabolic syndrome. J Chin Med Assoc. 2006;69(11):512-6. doi: 10.1016/s1726-4901(09)70320-x
  40. Rodríguez G, Soriano LC, Choi HK. Impact of diabetes against the future risk of developing gout. Ann Rheum Dis. 2010;69(12):2090-4. doi: 10.1136/ard.2010.130013
  41. Chen W, Liu X, Ye S. Effects of metformin on blood and urine proinflammatory mediators in patients with type 2 diabetes. J Inflamm (Lond). 2016;13:34. doi: 10.1186/s12950-016-0142-3
  42. Matsuura F, Yamashita S, Nakamura T, et al. Effects of visceral fat accumulation on uric acid metabolism in male obese subjects: visceral fat obesity is linked more closely to overproduction of uric acid than sub-cutaneous fat obesity. Metabolism. 1998;47:929-33. doi: 10.1016/S0026-0495(98)90346-8
  43. Chung YH, Kim DH, Lee WW. Monosodium urate crystal-induced pro-interleukin-1β production is post-transcriptionally regulated via the p38 signaling pathway in human monocytes. Sci Reports. 2016;6(1). doi: 10.1038/srep34533
  44. Vazirpanah N, Ottria A, van der Linden M, et al. mTOR inhibition by metformin impacts monosodium urate crystal-induced inflammation and cell death in gout: a prelude to a new add-on therapy? Ann Rheum Dis. 2019;78(5):663-71. doi: 10.1136/annrheumdis-2018-214656
  45. Мадянов И.В., Балаболкин М.И., Марков Д.С., Маркова Т.Н. Основные причины гиперурикемии при сахарном диабете. Терапевтический архив. 2000;72(2):55-8 [Madianov IV, Balabolkin MI, Markov DS, Markova TN. Main causes of hyperuricemia in diabetes mellitus. Therapeutic Archive. 2000;72(2):55-8 (In Russ.)].
  46. Feig DI. Uric Acid and Hypertension. Semin Nephrol. 2011;31(5):441-6. doi: 10.1016/j.semnephrol.2011.08.008
  47. Washburn WN, Poucher SM. Differentiating sodium-glucose co-transporter-2 inhibitors in development for the treatment of type 2 diabetes mellitus. Expert Opin Invest Drugs. 2013;22(4):463-86. doi: 10.1517/13543784.2013.774372
  48. Scheen AJ, Paquot N. Metabolic effects of SGLT-2 inhibitors beyond increased glucosuria: A review of the clinical evidence. Diabet Metab. 2014;40(6):S4-S11. doi: 10.1016/s1262-3636(14)72689-8
  49. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Intern Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
  50. Berhan A, Barker A. Sodium glucose co-transport 2 inhibitors in the treatment of type 2 diabetes mellitus: a meta-analysis of randomized double-blind controlled trials. BMC Endocrine Dis. 2013;13(1). doi: 10.1186/1472-6823-13-58
  51. Idris I, Donnelly R. Sodium-glucose co-transporter-2 inhibitors: an emerging new class of oral antidiabetic drug. Diabet Obes Metab. 2009;11(2):79-88. doi: 10.1111/j.1463-1326.2008.00982.x
  52. Kalra S. Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors: A Review of Their Basic and Clinical Pharmacology. Diabet Ther. 2014;5(2):355-66. doi: 10.1007/s13300-014-0089-4
  53. Дедов И.И., Шестакова М.В., Майоров А.Ю. и др. Алгоритмы специализированной медицинской помощи больным сахарным диабетом. 9-й вып. Сахарный диабет. 2019;22(1S1):1-144 [Dedov II, Shestakova, MV, Mayorov AY, et al. Standards of specialized diabetes care. 9th edition. Diabetes Mellitus. 2019;22(1S1):1-144 (In Russ.)]. doi: 10.14341/DM221S1
  54. List JF, Woo V, Morales E, et al. Sodium-Glucose Cotransport Inhibition With Dapagliflozin in Type 2 Diabetes. Diabetes Care. 2008;32(4):650-7. doi: 10.2337/dc08-1863
  55. Roden M, Merker L, Christiansen AV, et al. Safety, tolerability and effects on cardiometabolic risk factors of empagliflozin monotherapy in drug-naïve patients with type 2 diabetes: a double-blind extension of a Phase III randomized controlled trial. Cardiovasc Diabetol. 2015;14(1). doi: 10.1186/s12933-015-0314-0
  56. Davies MJ, Trujillo A, Vijapurkar U, et al. Effect of canagliflozin on serum uric acid in patients with type 2 diabetes mellitus. Diabet Obes Metab. 2015;17(4):426-9. doi: 10.1111/dom.12439
  57. Zhao Y, Xu L, Tian D, et al. Effects of sodium-glucose co-transporter 2 (SGLT2) inhibitors on serum uric acid level: A meta-analysis of randomized controlled trials. Diabet Obes Metab. 2017;20(2):458-62. doi: 10.1111/dom.13101
  58. Xin Y, Guo Y, Li Y, et al. Effects of sodium glucose cotransporter-2 inhibitors on serum uric acid in type 2 diabetes mellitus: A systematic review with an indirect comparison meta-analysis. Saudi J Biol Sci. 2019;26(2):421-6. doi: 10.1016/j.sjbs.2018.11.013
  59. Li J, Badve SV, Zhou Z, et al. The effects of canagliflozin on gout in type 2 diabetes: a post-hoc analysis of the CANVAS Program. Lancet Rheum. 2019;1(4):e220-e228. doi: 10.1016/s2665-9913(19)30078-5
  60. Chao EC. SGLT-2 Inhibitors: A New Mechanism for Glycemic Control. Clin Diabet. 2014;32(1):4-11. doi: 10.2337/diaclin.32.1.4
  61. Poudel R. Renal glucose handling in diabetes and sodium glucose cotransporter 2 inhibition. Ind J Endocrin Metab. 2013;17(4):588. doi: 10.4103/2230-8210.113725
  62. McGill JB. The SGLT2 Inhibitor Empagliflozin for the Treatment of Type 2 Diabetes Mellitus: a Bench to Bedside Review. Diabet Ther. 2014;5(1):43-63. doi: 10.1007/s13300-014-0063-1
  63. Doblado M, Moley KH. Facilitative glucose transporter 9, a unique hexose and urate transporter. Am J Physiol-Endocrinol Metab. 2009;297(4):E831-E835. doi: 10.1152/ajpendo.00296.2009
  64. Caulfield MJ, Munroe PB, O’Neill D, et al. SLC2A9 Is a High-Capacity Urate Transporter in Humans. Hattersley A, editor. PLoS Med. 2008;5(10):e197. doi: 10.1371/journal.pmed.0050197
  65. Chino Y, Samukawa Y, Sakai S, et al. SGLT2 inhibitor lowers serum uric acid through alteration of uric acid transport activity in renal tubule by increased glycosuria. Biopharm Drug Disposit. 2014;35(7):391-404. doi: 10.1002/bdd.1909
  66. Li S, Sanna S, Maschio A, et al. The GLUT9 Gene Is Associated with Serum Uric Acid Levels in Sardinia and Chianti Cohorts. PLoS Genet. 2007;3(11):e194. doi: 10.1371/journal.pgen.0030194
  67. Satirapoj B, Adler SG. Comprehensive approach to diabetic nephropathy. Kidney Res Clin Pract. 2014;33:121-31. doi: 10.1016/j.krcp.2014.08.001
  68. Maeda S, Matsui T, Takeuchi M, Yamagishi S. Sodium-glucose cotransporter 2-mediated oxidative stress augments advanced glycation end products-induced tubular cell apoptosis. Diabet Metab Res Rev. 2013;29(5):406-12. doi: 10.1002/dmrr.2407
  69. 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
  70. Ojima A, Matsui T, Nishino Y, et al. Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis. Hormone Metab Res. 2015;47(09):686-92. doi: 10.1055/s-0034-1395609
  71. Dekkers CJ, Petrykiv S, Laverman GD, et al. Effects of the SGLT-2 inhibitor dapagliflozin on glomerular and tubular injury markers. Diabet Obes Metab. 2018;20(8):1988-93. doi: 10.1111/dom.13301
  72. Shimazu T, Hirschey MD, Newman J, et al. Suppression of Oxidative Stress by-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor. Science. 2012;339(6116):211-4. doi: 10.1126/science.1227166
  73. Hill NR, Fatoba ST, Oke JL, et al. Global Prevalence of Chronic Kidney Disease – A Systematic Review and Meta-Analysis. Remuzzi G, editor. PLOS One. 2016;11(7):e0158765. doi: 10.1371/journal.pone.0158765
  74. Vallon V, Gerasimova M, Rose MA, et al. SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice. Am J Physiol-Renal Physiol. 2014;306(2):F194-F204. doi: 10.1152/ajprenal.00520.2013
  75. Liao X, Wang X, Li H, et al. Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Increases Circulating Zinc-Α2-Glycoprotein Levels in Patients with Type 2 Diabetes. Sci Reports. 2016;6(1). doi: 10.1038/srep32887
  76. Mancini SJ, Boyd D, Katwan OJ, et al. Canagliflozin inhibits interleukin-1β-stimulated cytokine and chemokine secretion in vascular endothelial cells by AMP-activated protein kinase-dependent and -independent mechanisms. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-23420-4
  77. Maldonado-Cervantes MI, Galicia OG, Moreno-Jaime B, et al. Autocrine modulation of glucose transporter SGLT2 by IL-6 and TNF-α in LLC-PK1 cells. J Physiol Biochem. 2012;68(3):411-20. doi: 10.1007/s13105-012-0153-3
  78. Scheen AJ, Van Gaal LF. Combating the dual burden: therapeutic targeting of common pathways in obesity and type 2 diabetes. Lancet Diabet Endocrinol. 2014;2(11):911-22. doi: 10.1016/s2213-8587(14)70004-x
  79. Barnett AH. Impact of sodium glucose cotransporter 2 inhibitors on weight in patients with type 2 diabetes mellitus. Postgrad Med. 2013;125:92-100. doi: 10.3810/pgm.2013.09.2698
  80. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Int Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
  81. Liu X-Y, Zhang N, Chen R, et al. Efficacy and safety of sodium–glucose cotransporter 2 inhibitors in type 2 diabetes: a meta-analysis of randomized controlled trials for 1 to 2 years. J Diabet Complicat. 2015;29(8):1295-303. doi: 10.1016/j.jdiacomp.2015.07.011
  82. Ferrannini G, Hach T, Crowe S, et al. Energy Balance After Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1730-5. doi: 10.2337/dc15-0355
  83. Ladwig K-H, Marten-Mittag B, Löwel H, et al. Influence of depressive mood on the association of CRP and obesity in 3205 middle aged healthy men. Brain, Behav Immun. 2003;17(4):268-75. doi: 10.1016/s0889-1591(03)00056-4
  84. Bochud M, Marquant F, Marques-Vidal P-M, et al. Association between C-Reactive Protein and Adiposity in Women. J Clin Endocrinol Metab. 2009;94(10):3969-77. doi: 10.1210/jc.2008-2428
  85. Jung U, Choi M-S. Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease. Int J Mol Sci. 2014;15(4):6184-223. doi: 10.3390/ijms15046184
  86. Yaribeygi H, Butler AE, Atkin SL, et al. Sodium-glucose cotransporter 2 inhibitors and inflammation in chronic kidney disease: Possible molecular pathways. J Cell Physiol. 2018;234(1):223-30. doi: 10.1002/jcp.26851
  87. Kuriyama S. Protection of the kidney with sodium-glucose cotransporter 2 inhibitors: potential mechanisms raised by the large-scaled randomized control trials. Clin Exper Nephrol. 2018;23(3):304-12. doi: 10.1007/s10157-018-1673-0
  88. Maliha G, Townsend RR. SGLT2 inhibitors: their potential reduction in blood pressure. J Am Soc Hypertens. 2015;9(1):48-53. doi: 10.1016/j.jash.2014.11.001
  89. Baker WL, Smyth LR, Riche DM, et al. Effects of sodium-glucose co-transporter 2 inhibitors on blood pressure: A systematic review and meta-analysis. J Am Soc Hypertens. 2014;8(4):262-75.e9. doi: 10.1016/j.jash.2014.01.007
  90. Sano M, Chen S, Imazeki H, et al. Changes in heart rate in patients with type 2 diabetes mellitus after treatment with luseogliflozin: Subanalysis of placebo-controlled, double-blind clinical trials. J Diabet Invest. 2018;9(3):638-41. doi: 10.1111/jdi.12726
  91. Wu JHY, Foote C, Blomster J, et al. Effects of sodium-glucose cotransporter-2 inhibitors on cardiovascular events, death, and major safety outcomes in adults with type 2 diabetes: a systematic review and meta-analysis. Lancet Diabet Endocrinol. 2016;4(5):411-9. doi: 10.1016/s2213-8587(16)00052-8
  92. Ptaszynska A, Johnsson KM, Parikh SJ, et al. Safety Profile of Dapagliflozin for Type 2 Diabetes: Pooled Analysis of Clinical Studies for Overall Safety and Rare Events. Drug Safety. 2014;37(10):815-29. doi: 10.1007/s40264-014-0213-4
  93. Johnsson KM, Ptaszynska A, Schmitz B, et al. Urinary tract infections in patients with diabetes treated with dapagliflozin. J Diabet Complicat. 2013;27:473-8. doi: 10.1016/j.jdiacomp.2013.05.004
  94. Peters AL, Buschur EO, Buse JB, et al. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1687-93. doi: 10.2337/dc15-0843
  95. Bonner C, Kerr-Conte J, Gmyr V, et al. Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. Nature Med. 2015;21(5):512-7. doi: 10.1038/nm.3828
  96. Kalra S, Gupta Y, Patil S. Sodium-glucose cotransporter-2 inhibition and the insulin: Glucagon ratio: Unexplored dimensions. Ind J Endocrinol Metab. 2015;19(3):426. doi: 10.4103/2230-8210.152793
  97. Rosenstock J, Ferrannini E. Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors. Diabet Care. 2015;38(9):1638-42. doi: 10.2337/dc15-1380
  98. Zhang M, Zhang L, Wu B, et al. Dapagliflozin treatment for type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials. Diabet/Metab Res Rev. 2014;30(3):204-21. doi: 10.1002/dmrr.2479
  99. Meier C, Schwartz AV, Egger A, Lecka-Czernik B. Effects of diabetes drugs on the skeleton. Bone. 2016;82:93-100. doi: 10.1016/j.bone.2015.04.026
  100. Ljunggren Ö, Bolinder J, Johansson L, et al. Dapagliflozin has no effect on markers of bone formation and resorption or bone mineral density in patients with inadequately controlled type 2 diabetes mellitus on metformin. Diabet Obes Metab. 2012;14(11):990-9. doi: 10.1111/j.1463-1326.2012.01630.x
  101. Bolinder J, Ljunggren Ö, Johansson L, et al. Dapagliflozin maintains glycaemic control while reducing weight and body fat mass over 2 years in patients with type 2 diabetes mellitus inadequately controlled on metformin. Diabet Obes Metab. 2013;16(2):159-69. doi: 10.1111/dom.12189
  102. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. New Engl J Med. 2015;373(22):2117-28. doi: 10.1056/nejmoa1504720
  103. Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes. New Engl J Med. 2016;375(4):323-34. doi: 10.1056/nejmoa1515920
  104. Ptaszynska A, Cohen SM, Messing EM, et al. Assessing Bladder Cancer Risk in Type 2 Diabetes Clinical Trials: the Dapagliflozin Drug Development Program as a «Case Study». Diabet Ther. 2015;6(3):357-75. doi: 10.1007/s13300-015-0128-9
  105. Yang H-C, Nguyen PAA, Islam M, et al. Gout drugs use and risk of cancer: A case-control study. Joint Bone Spine. 2018;85(6):747-53. doi: 10.1016/j.jbspin.2018.01.008
  106. Lin H-W, Tseng C-H. A Review on the Relationship between SGLT2 Inhibitors and Cancer. Int J Endocrinol. 2014;2014:1-6. doi: 10.1155/2014/719578
  107. Neal B, Perkovic V, Mahaffey KW, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. New Engl J Med. 2017;377(7):644-57. doi: 10.1056/nejmoa1611925
  108. Hallow KM, Helmlinger G, Greasley PJ, et al. Why do SGLT2 inhibitors reduce heart failure hospitalization? A differential volume regulation hypothesis. Diabet Obes Metab. 2018;20(3):479-87. doi: 10.1111/dom.13126

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