NON-ALCOHOLIC FATTY LIVER DISEASE AND TYPE 2 DIABETES: THE PROBLEM OF ASSOCIATION AND STAGES OF DEVELOPMENT
Keywords:
non-alcoholic fatty liver disease, type 2 diabetes mellitus, obesity, insulin resistance, metabolic syndrome, FAFLD
Abstract
The wide prevalence of non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (DM2), as well as their relationship, determines the need for targeted consideration of this pathology in order to optimize approaches to the diagnosis and treatment of patients with NAFLD and type 2 diabetes. Being components of the metabolic syndrome, these two diseases have largely similar mechanisms of development and progression, synergistically increasing the risk of adverse outcomes in comorbid patients. Despite the commonality of pathophysiological mechanisms, the question of the sequence of development of NAFLD and T2DM remains relevant.
Based on the results of the analysis of the literature, two main theories were identified: alimentary and metabolic. According to the alimentary theory, the primary link in the pathogenesis is obesity and the associated excessive accumulation of free fatty acids and triglycerides in the liver, which subsequently leads to insulin resistance and the development of type 2 diabetes. In contrast, the metabolic theory considers the insulin resistance associated with diabetes to be the primary blow, which, regardless of obesity, creates the prerequisites for liver damage. In addition, the review pays special attention to the consideration of a new concept - metabolically associated fatty liver disease (MAFLD), considered as a hepatic component of the metabolic syndrome. Within the framework of this concept, various clinical phenotypes of NAFLD are distinguished, which determine the path along which the diseases under consideration develop. In conclusion, the review discusses pathogenetically based therapy, which focuses on overcoming insulin resistance, correcting atherogenic dyslipidemia, and restoring the structure and function of liver cells.
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References
1. ↑1. В Who.int [Internet]. The top 10 causes of death [cited 2020 9 Dec]. Available from: https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death
2. ↑2. Ротберг Г.Е., ред. Метаболический синдром. - М.: МЕД-М54 пресс-информ; 2007.
3. ↑3. Ланг Г.Ф. Гипертоническая болезнь. - Л.: Медгиз; 1950.
4. ↑4. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988;37(12):1595-1607. https://doi.org/10.2337/diab.37.12.1595
5. ↑5. D’Adamo E, Marcovecchio ML, Giannini C, et al. The possible role of liver steatosis in defining metabolic syndrome in prepubertal children. Metabolism. 2010;59:671-676. https://doi.org/10.1016/j.metabol.2009.09.012
6. ↑6. Belenkov Yu.N., Privalova E.V., Kaplunova V.Yu., et al. Metabolic syndrome: history of development, main diagnostic criteria // Rational pharmacotherapy in cardiology. - 2018. - V. 14. - No. 5. - S. 757-765.
7. ↑7. Lazabnik L.B., Golovanova E.V., Turkina S.V., et al. Non-alcoholic fatty liver disease in adults: clinic, diagnosis, treatment. Recommendations for therapists, third version // Experimental and clinical gastroenterology. - 2021. - Vol. 1. - No. 1. - pp. 4-52.
8. ↑8. Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73-84. https://doi.org/10.1002/hep.28431
9. ↑9. Younossi ZM, Blissett D, Blissett R, et al. The economic and clinical burden of nonalcoholic fatty liver disease in the United States and Europe. Hepatology. 2016;64(5):1577-1586. https://doi.org/10.1002/hep.28785
10. ↑10. de Alwis NM, Day CP. Non-alcoholic fatty liver disease: the mist gradually clears. J Hepatol. 2008;48 Suppl 1:S104-S112. https://doi.org/10.1016/j.jhep.2008.01.009
11. ↑11. Sanyal AJ; American Gastroenterological Association. AGA technical review on nonalcoholic fatty liver disease. Gastroenterology. 2002;123(5):1705-1725. https://doi.org/10.1053/gast.2002.36572
12. ↑12. Eslam M, Sanyal AJ, George J; International Consensus Panel. MAFLD: A Consensus-Driven Proposed Nomenclature for Metabolic Associated Fatty Liver Disease. Gastroenterology. 2020;158(7):1999-2014.e1. https://doi.org/10.1053/j.gastro.2019.11.312
13. ↑13. International Diabetes Federation. IDF Diabetes Atlas. 9th ed. Brussels: IDF; 2019; 176 p.
14. ↑14. Idf.org [Internet]. One adult in ten will have diabetes by 2030. International Diabetes Federation [cited 2011 Nov 14]. Available from: http://www.idf.org media-events/press-releases/2011/diabetes-atlas-5th-edition
15. ↑15. Younossi ZM, Golabi P, de Avila L, et al. The global epidemiology of NAFLD and NASH in patients with type 2 diabetes: A systematic review and meta-analysis. J Hepatol. 2019;71(4):793-801. https://doi.org/10.1016/j.jhep.2019.06.021
16. ↑16. Targher G, Bertolini L, Padovani R, et al. Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care. 2007;30(5):1212-1218. https://doi.org/10.2337/dc06-2247
17. ↑17. Targher G. Is it time for non-alcoholic fatty liver disease screening in patients with type 2 diabetes mellitus? Hepatobiliary Surg Nutr. 2020;9(2):239-241. https://doi.org/10.21037/hbsn.2019.10.21
18. ↑18. Younossi ZM, Gramlich T, Matteoni CA, et al. Nonalcoholic fatty liver disease in patients with type 2 diabetes [published correction appears in Clin Gastroenterol Hepatol. 2004 Jun;2(6):522]. Clin Gastroenterol Hepatol. 2004;2(3):262-265. https://doi.org/10.1016/s1542-3565(04)00014-x
19. ↑19. Hossain N, Afendy A, Stepanova M, et al. Independent predictors of fibrosis in patients with nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol. 2009;7(11):1224-1229.e12292. https://doi.org/10.1016/j.cgh.2009.06.007
20. ↑20. Stepanova M, Rafiq N, Makhlouf H, et al. Predictors of all-cause mortality and liver-related mortality in patients with non-alcoholic fatty liver disease (NAFLD). Dig Dis Sci. 2013;58(10):3017-3023. https://doi.org/10.1007/s10620-013-2743-5
21. ↑21. Fracanzani AL, Valenti L, Bugianesi E, et al. Risk of severe liver disease in nonalcoholic fatty liver disease with normal aminotransferase levels: a role for insulin resistance and diabetes. Hepatology. 2008;48(3):792-798. https://doi.org/10.1002/hep.22429
22. ↑22. Mofrad P, Contos MJ, Haque M, et al. Clinical and histologic spectrum of nonalcoholic fatty liver disease associated with normal ALT values. Hepatology. 2003;37(6):1286-1292. https://doi.org/10.1053/jhep.2003.50229
23. ↑23. Leitner DR, Frühbeck G, Yumuk V, et al. Obesity and Type 2 Diabetes: Two Diseases with a Need for Combined Treatment Strategies - EASO Can Lead the Way. Obes Facts. 2017;10(5):483-492. https://doi.org/10.1159/000480525
24. ↑24. Wang HH, Lee DK, Liu M, Portincasa P, Wang DQ. Novel Insights into the Pathogenesis and Management of the Metabolic Syndrome. Pediatr Gastroenterol Hepatol Nutr. 2020;23(3):189-230. https://doi.org/10.5223/pghn.2020.23.3.189
25. ↑25. Bae JC, Cho YK, Lee WY, et al. Impact of nonalcoholic fatty liver disease on insulin resistance in relation to HbA1c levels in nondiabetic subjects. Am J Gastroenterol. 2010;105(11):2389-2395. https://doi.org/10.1038/ajg.2010.275
26. ↑26. Dongiovanni P, Stender S, Pietrelli A, et al. Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver. J Intern Med. 2018;283(4):356-370. https://doi.org/10.1111/joim.12719
27. ↑27. Manchanayake J, Chitturi S, Nolan C, Farrell GC. Postprandial hyperinsulinemia is universal in non-diabetic patients with nonalcoholic fatty liver disease. J Gastroenterol Hepatol. 2011;26(3):510-516. https://doi.org/10.1111/j.1440-1746.2010.06528.x
28. ↑28. Bakulin I.G., Sandler Yu.G., Vinnitskaya E.V., et al. Diabetes mellitus and non-alcoholic fatty liver disease: facets of conjugation // Therapeutic archive. - 2017. - T. 89. - No. 2. - S. 59-65.
29. ↑29. De Bruyne RM, Fitzpatrick E, Dhawan A. Fatty liver disease in children: eat now pay later. Hepatol Int. 2010;4(1):375-385. Published 2010 Jan 29. https://doi.org/10.1007/s12072-009-9160-z
30. ↑30. Drapkina O.M., Korneeva O.N., Ivashkin V.T. Therapy of non-alcoholic steatohepatitis in metabolic syndrome: focus on essential phospholipids // Attending physician. - 2010. - No. 2. - S. 18-24.
31. ↑31. European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-1402. https://doi.org/10.1016/j.jhep.2015.11.004
32. ↑32. Lavrenova E.A., Drapkina O.M. Insulin resistance in obesity: causes and consequences // Obesity and metabolism. - 2020. - V. 17. - No. 1. - C. 48-55.
33. ↑33. Babenko A.Yu., Laevskaya M.Yu. Non-alcoholic fatty liver disease - relationship with metabolic syndrome // Russian Medical Journal. - 2018. - Vol. 1. - No. I. - S. 34-4
34. ↑34. Ding X, Saxena NK, Lin S, et al. Exendin-4, a glucagon-like protein-1 (GLP-1) receptor agonist, reverses hepatic steatosis in ob/ob mice. Hepatology. 2006;43(1):173-81.
35. ↑35. Marchesini G, Brizi M, Morselli-Labate AM, et al. Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med. 1999;107(5):450-455. https://doi.org/ 10.1016/s0002-9343(99)00271-5
36. ↑36. Watt MJ, Miotto PM, De Nardo W, Montgomery MK. The Liver as an Endocrine Organ-Linking NAFLD and Insulin Resistance. Endocr Rev. 2019;40(5):1367-1393. https://doi.org/10.1210/er.2019-00034
37. ↑37. Stefan N, Fritsche A, Weikert C, et al. Plasma fetuin-A levels and the risk of type 2 diabetes. Diabetes. 2008;57(10):2762-7. https://doi.org/10.2337/db08-0538
38. ↑38. Hussey SE, Liang H, Costford SR, et al. TAK-242, a small-molecule inhibitor of Toll-like receptor 4 signalling, unveils similarities and differences in lipopolysaccharide- and lipid-induced inflammation and insulin resistance in muscle cells. Biosci Rep. 2012;33(1):37-47. https://doi.org/10.1042/BSR20120098
39. ↑39. Kytikova O.Yu., Novgorodtseva T.P., Denisenko Yu.K., et al. Toll-like receptors in the pathophysiology of obesity // Obesity and Metabolism. - 2020. - V. 17. - No. 1. - C. 56-63.
40. ↑40. Butrova S.A. Metabolic syndrome: pathogenesis, clinic, diagnosis, approaches to treatment // Russian Medical Journal. - 2001. - No. 2. - S. 56-8.↑41. Seppälä-Lindroos A, Vehkavaara S, Häkkinen AM, et al. Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. J Clin Endocrinol Metab. 2002;87(7):3023-3028. https://doi.org/10.1210/jcem.87.7.8638
41. ↑42. Valenti L, Bugianesi E, Pajvani U, Targher G. Nonalcoholic fatty liver disease: cause or consequence of type 2 diabetes? Liver Int. 2016;36(11):1563-1579. https://doi.org/10.1111/liv.13185
42. ↑43. Pavlenko O.A. Obesity as a risk factor for non-alcoholic fatty liver disease. Almanac of Clinical Medicine. - 2015. - Vol. 1. - No. 1. - S. 60-66.
43. ↑44. Mishina E.E., Maiorov A.Yu., Bogomolov P.O., et al. Non-alcoholic fatty liver disease: a cause or consequence of insulin resistance? // Diabetes. - 2017. - T. 20. - No. 5. - S. 335-342.
44. ↑45. Petersen KF, Dufour S, Savage DB, et al. The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Proc Natl Acad Sci U S A. 2007;104(31):12587-12594. https://doi.org/10.1073/pnas.0705408104
45. ↑46. Younossi Z, Anstee QM, Marietti M, et al. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018;15(1):11-20. https://doi.org/10.1038/nrgastro.2017.109
46. ↑47. Das K, Chowdhury A. Lean NASH: distinctiveness and clinical implication. Hepatol Int. 2013;7 Suppl 2:806-813. https://doi.org/10.1007/s12072-013-9477-5
47. ↑48. Eckel N, Li Y, Kuxhaus O, et al. Transition from metabolic healthy to unhealthy phenotypes and association with cardiovascular disease risk across BMI categories in 90 257 women (the Nurses’ Health Study): 30 year follow-up from a prospective cohort study. Lancet Diabetes Endocrinol. 2018;6(9):714-724. https://doi.org/10.1016/S2213-8587(18)30137-2
48. ↑49. Caleyachetty R, Thomas GN, Toulis KA, et al. Metabolically Healthy Obese and Incident Cardiovascular Disease Events Among 3.5 Million Men and Women. J Am Coll Cardiol. 2017;70(12):1429-1437. https://doi.org/10.1016/j.jacc.2017.07.763
49. ↑50. Lassale C, Tzoulaki I, Moons KGM, et al. Separate and combined associations of obesity and metabolic health with coronary heart disease: a pan-European case-cohort analysis. Eur Heart J. 2018;39(5):397-406. https://doi.org/10.1093/eurheartj/ehx448
50. ↑51. Drapkina O.M. Non-alcoholic fatty liver disease and metabolic syndrome // Handbook of a polyclinic doctor. - 2008. - No. 3. - S. 71-74.
51. ↑52. European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-1402. https://doi.org/10.1016/j.jhep.2015.11.004
52. ↑53. Whitsett M, VanWagner LB. Physical activity as a treatment of non-alcoholic fatty liver disease: A systematic review. World J Hepatol. 2015;7(16):2041-2052. https://doi.org/10.4254/wjh.v7.i16.2041
53. ↑54. Borghouts LB, Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000;21(1):1-12. https://doi.org/10.1055/s-2000-8847
54. ↑55. Golabi et al. Effectiveness of exercise in hepatic fat mobilization in nonalcoholic fatty liver disease: Systematic review. World J Gastroenterol. 2016;22(27):6318-632
55. ↑56. Wang ST, Zheng J, Peng HW, et al. Physical activity intervention for non-diabetic patients with non-alcoholic fatty liver disease: a meta-analysis of randomized controlled trials. BMC Gastroenterol. 2020;20(1):66. Published 2020 Mar 12. https://doi.org/ 10.1186/s12876-020-01204-3
56. ↑57. Zhou J, Massey S, Story D, Li L. Metformin: An Old Drug with New Applications. Int J Mol Sci. 2018;19(10):2863. https://doi.org/ 10.3390/ijms19102863
2. ↑2. Ротберг Г.Е., ред. Метаболический синдром. - М.: МЕД-М54 пресс-информ; 2007.
3. ↑3. Ланг Г.Ф. Гипертоническая болезнь. - Л.: Медгиз; 1950.
4. ↑4. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988;37(12):1595-1607. https://doi.org/10.2337/diab.37.12.1595
5. ↑5. D’Adamo E, Marcovecchio ML, Giannini C, et al. The possible role of liver steatosis in defining metabolic syndrome in prepubertal children. Metabolism. 2010;59:671-676. https://doi.org/10.1016/j.metabol.2009.09.012
6. ↑6. Belenkov Yu.N., Privalova E.V., Kaplunova V.Yu., et al. Metabolic syndrome: history of development, main diagnostic criteria // Rational pharmacotherapy in cardiology. - 2018. - V. 14. - No. 5. - S. 757-765.
7. ↑7. Lazabnik L.B., Golovanova E.V., Turkina S.V., et al. Non-alcoholic fatty liver disease in adults: clinic, diagnosis, treatment. Recommendations for therapists, third version // Experimental and clinical gastroenterology. - 2021. - Vol. 1. - No. 1. - pp. 4-52.
8. ↑8. Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73-84. https://doi.org/10.1002/hep.28431
9. ↑9. Younossi ZM, Blissett D, Blissett R, et al. The economic and clinical burden of nonalcoholic fatty liver disease in the United States and Europe. Hepatology. 2016;64(5):1577-1586. https://doi.org/10.1002/hep.28785
10. ↑10. de Alwis NM, Day CP. Non-alcoholic fatty liver disease: the mist gradually clears. J Hepatol. 2008;48 Suppl 1:S104-S112. https://doi.org/10.1016/j.jhep.2008.01.009
11. ↑11. Sanyal AJ; American Gastroenterological Association. AGA technical review on nonalcoholic fatty liver disease. Gastroenterology. 2002;123(5):1705-1725. https://doi.org/10.1053/gast.2002.36572
12. ↑12. Eslam M, Sanyal AJ, George J; International Consensus Panel. MAFLD: A Consensus-Driven Proposed Nomenclature for Metabolic Associated Fatty Liver Disease. Gastroenterology. 2020;158(7):1999-2014.e1. https://doi.org/10.1053/j.gastro.2019.11.312
13. ↑13. International Diabetes Federation. IDF Diabetes Atlas. 9th ed. Brussels: IDF; 2019; 176 p.
14. ↑14. Idf.org [Internet]. One adult in ten will have diabetes by 2030. International Diabetes Federation [cited 2011 Nov 14]. Available from: http://www.idf.org media-events/press-releases/2011/diabetes-atlas-5th-edition
15. ↑15. Younossi ZM, Golabi P, de Avila L, et al. The global epidemiology of NAFLD and NASH in patients with type 2 diabetes: A systematic review and meta-analysis. J Hepatol. 2019;71(4):793-801. https://doi.org/10.1016/j.jhep.2019.06.021
16. ↑16. Targher G, Bertolini L, Padovani R, et al. Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care. 2007;30(5):1212-1218. https://doi.org/10.2337/dc06-2247
17. ↑17. Targher G. Is it time for non-alcoholic fatty liver disease screening in patients with type 2 diabetes mellitus? Hepatobiliary Surg Nutr. 2020;9(2):239-241. https://doi.org/10.21037/hbsn.2019.10.21
18. ↑18. Younossi ZM, Gramlich T, Matteoni CA, et al. Nonalcoholic fatty liver disease in patients with type 2 diabetes [published correction appears in Clin Gastroenterol Hepatol. 2004 Jun;2(6):522]. Clin Gastroenterol Hepatol. 2004;2(3):262-265. https://doi.org/10.1016/s1542-3565(04)00014-x
19. ↑19. Hossain N, Afendy A, Stepanova M, et al. Independent predictors of fibrosis in patients with nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol. 2009;7(11):1224-1229.e12292. https://doi.org/10.1016/j.cgh.2009.06.007
20. ↑20. Stepanova M, Rafiq N, Makhlouf H, et al. Predictors of all-cause mortality and liver-related mortality in patients with non-alcoholic fatty liver disease (NAFLD). Dig Dis Sci. 2013;58(10):3017-3023. https://doi.org/10.1007/s10620-013-2743-5
21. ↑21. Fracanzani AL, Valenti L, Bugianesi E, et al. Risk of severe liver disease in nonalcoholic fatty liver disease with normal aminotransferase levels: a role for insulin resistance and diabetes. Hepatology. 2008;48(3):792-798. https://doi.org/10.1002/hep.22429
22. ↑22. Mofrad P, Contos MJ, Haque M, et al. Clinical and histologic spectrum of nonalcoholic fatty liver disease associated with normal ALT values. Hepatology. 2003;37(6):1286-1292. https://doi.org/10.1053/jhep.2003.50229
23. ↑23. Leitner DR, Frühbeck G, Yumuk V, et al. Obesity and Type 2 Diabetes: Two Diseases with a Need for Combined Treatment Strategies - EASO Can Lead the Way. Obes Facts. 2017;10(5):483-492. https://doi.org/10.1159/000480525
24. ↑24. Wang HH, Lee DK, Liu M, Portincasa P, Wang DQ. Novel Insights into the Pathogenesis and Management of the Metabolic Syndrome. Pediatr Gastroenterol Hepatol Nutr. 2020;23(3):189-230. https://doi.org/10.5223/pghn.2020.23.3.189
25. ↑25. Bae JC, Cho YK, Lee WY, et al. Impact of nonalcoholic fatty liver disease on insulin resistance in relation to HbA1c levels in nondiabetic subjects. Am J Gastroenterol. 2010;105(11):2389-2395. https://doi.org/10.1038/ajg.2010.275
26. ↑26. Dongiovanni P, Stender S, Pietrelli A, et al. Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver. J Intern Med. 2018;283(4):356-370. https://doi.org/10.1111/joim.12719
27. ↑27. Manchanayake J, Chitturi S, Nolan C, Farrell GC. Postprandial hyperinsulinemia is universal in non-diabetic patients with nonalcoholic fatty liver disease. J Gastroenterol Hepatol. 2011;26(3):510-516. https://doi.org/10.1111/j.1440-1746.2010.06528.x
28. ↑28. Bakulin I.G., Sandler Yu.G., Vinnitskaya E.V., et al. Diabetes mellitus and non-alcoholic fatty liver disease: facets of conjugation // Therapeutic archive. - 2017. - T. 89. - No. 2. - S. 59-65.
29. ↑29. De Bruyne RM, Fitzpatrick E, Dhawan A. Fatty liver disease in children: eat now pay later. Hepatol Int. 2010;4(1):375-385. Published 2010 Jan 29. https://doi.org/10.1007/s12072-009-9160-z
30. ↑30. Drapkina O.M., Korneeva O.N., Ivashkin V.T. Therapy of non-alcoholic steatohepatitis in metabolic syndrome: focus on essential phospholipids // Attending physician. - 2010. - No. 2. - S. 18-24.
31. ↑31. European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-1402. https://doi.org/10.1016/j.jhep.2015.11.004
32. ↑32. Lavrenova E.A., Drapkina O.M. Insulin resistance in obesity: causes and consequences // Obesity and metabolism. - 2020. - V. 17. - No. 1. - C. 48-55.
33. ↑33. Babenko A.Yu., Laevskaya M.Yu. Non-alcoholic fatty liver disease - relationship with metabolic syndrome // Russian Medical Journal. - 2018. - Vol. 1. - No. I. - S. 34-4
34. ↑34. Ding X, Saxena NK, Lin S, et al. Exendin-4, a glucagon-like protein-1 (GLP-1) receptor agonist, reverses hepatic steatosis in ob/ob mice. Hepatology. 2006;43(1):173-81.
35. ↑35. Marchesini G, Brizi M, Morselli-Labate AM, et al. Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med. 1999;107(5):450-455. https://doi.org/ 10.1016/s0002-9343(99)00271-5
36. ↑36. Watt MJ, Miotto PM, De Nardo W, Montgomery MK. The Liver as an Endocrine Organ-Linking NAFLD and Insulin Resistance. Endocr Rev. 2019;40(5):1367-1393. https://doi.org/10.1210/er.2019-00034
37. ↑37. Stefan N, Fritsche A, Weikert C, et al. Plasma fetuin-A levels and the risk of type 2 diabetes. Diabetes. 2008;57(10):2762-7. https://doi.org/10.2337/db08-0538
38. ↑38. Hussey SE, Liang H, Costford SR, et al. TAK-242, a small-molecule inhibitor of Toll-like receptor 4 signalling, unveils similarities and differences in lipopolysaccharide- and lipid-induced inflammation and insulin resistance in muscle cells. Biosci Rep. 2012;33(1):37-47. https://doi.org/10.1042/BSR20120098
39. ↑39. Kytikova O.Yu., Novgorodtseva T.P., Denisenko Yu.K., et al. Toll-like receptors in the pathophysiology of obesity // Obesity and Metabolism. - 2020. - V. 17. - No. 1. - C. 56-63.
40. ↑40. Butrova S.A. Metabolic syndrome: pathogenesis, clinic, diagnosis, approaches to treatment // Russian Medical Journal. - 2001. - No. 2. - S. 56-8.↑41. Seppälä-Lindroos A, Vehkavaara S, Häkkinen AM, et al. Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. J Clin Endocrinol Metab. 2002;87(7):3023-3028. https://doi.org/10.1210/jcem.87.7.8638
41. ↑42. Valenti L, Bugianesi E, Pajvani U, Targher G. Nonalcoholic fatty liver disease: cause or consequence of type 2 diabetes? Liver Int. 2016;36(11):1563-1579. https://doi.org/10.1111/liv.13185
42. ↑43. Pavlenko O.A. Obesity as a risk factor for non-alcoholic fatty liver disease. Almanac of Clinical Medicine. - 2015. - Vol. 1. - No. 1. - S. 60-66.
43. ↑44. Mishina E.E., Maiorov A.Yu., Bogomolov P.O., et al. Non-alcoholic fatty liver disease: a cause or consequence of insulin resistance? // Diabetes. - 2017. - T. 20. - No. 5. - S. 335-342.
44. ↑45. Petersen KF, Dufour S, Savage DB, et al. The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Proc Natl Acad Sci U S A. 2007;104(31):12587-12594. https://doi.org/10.1073/pnas.0705408104
45. ↑46. Younossi Z, Anstee QM, Marietti M, et al. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018;15(1):11-20. https://doi.org/10.1038/nrgastro.2017.109
46. ↑47. Das K, Chowdhury A. Lean NASH: distinctiveness and clinical implication. Hepatol Int. 2013;7 Suppl 2:806-813. https://doi.org/10.1007/s12072-013-9477-5
47. ↑48. Eckel N, Li Y, Kuxhaus O, et al. Transition from metabolic healthy to unhealthy phenotypes and association with cardiovascular disease risk across BMI categories in 90 257 women (the Nurses’ Health Study): 30 year follow-up from a prospective cohort study. Lancet Diabetes Endocrinol. 2018;6(9):714-724. https://doi.org/10.1016/S2213-8587(18)30137-2
48. ↑49. Caleyachetty R, Thomas GN, Toulis KA, et al. Metabolically Healthy Obese and Incident Cardiovascular Disease Events Among 3.5 Million Men and Women. J Am Coll Cardiol. 2017;70(12):1429-1437. https://doi.org/10.1016/j.jacc.2017.07.763
49. ↑50. Lassale C, Tzoulaki I, Moons KGM, et al. Separate and combined associations of obesity and metabolic health with coronary heart disease: a pan-European case-cohort analysis. Eur Heart J. 2018;39(5):397-406. https://doi.org/10.1093/eurheartj/ehx448
50. ↑51. Drapkina O.M. Non-alcoholic fatty liver disease and metabolic syndrome // Handbook of a polyclinic doctor. - 2008. - No. 3. - S. 71-74.
51. ↑52. European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-1402. https://doi.org/10.1016/j.jhep.2015.11.004
52. ↑53. Whitsett M, VanWagner LB. Physical activity as a treatment of non-alcoholic fatty liver disease: A systematic review. World J Hepatol. 2015;7(16):2041-2052. https://doi.org/10.4254/wjh.v7.i16.2041
53. ↑54. Borghouts LB, Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000;21(1):1-12. https://doi.org/10.1055/s-2000-8847
54. ↑55. Golabi et al. Effectiveness of exercise in hepatic fat mobilization in nonalcoholic fatty liver disease: Systematic review. World J Gastroenterol. 2016;22(27):6318-632
55. ↑56. Wang ST, Zheng J, Peng HW, et al. Physical activity intervention for non-diabetic patients with non-alcoholic fatty liver disease: a meta-analysis of randomized controlled trials. BMC Gastroenterol. 2020;20(1):66. Published 2020 Mar 12. https://doi.org/ 10.1186/s12876-020-01204-3
56. ↑57. Zhou J, Massey S, Story D, Li L. Metformin: An Old Drug with New Applications. Int J Mol Sci. 2018;19(10):2863. https://doi.org/ 10.3390/ijms19102863
Published
2022-10-28
How to Cite
Badridinova B.K. (2022). NON-ALCOHOLIC FATTY LIVER DISEASE AND TYPE 2 DIABETES: THE PROBLEM OF ASSOCIATION AND STAGES OF DEVELOPMENT. Central Asian Journal of Theoretical and Applied Science, 3(10), 246-255. Retrieved from https://cajotas.centralasianstudies.org/index.php/CAJOTAS/article/view/971
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