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Экспериментальная и клиническая гастроэнтерология

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РОЛЬ АДИПОЦИТОКИНОВ, ГРЕЛИНА И ИНКРЕТИНОВ В ПРЕДИКЦИИ НЕАЛКОГОЛЬНОЙ ЖИРОВОЙ БОЛЕЗНИ ПЕЧЕНИ И ЕЕ ЛЕЧЕНИИ У ПАЦИЕНТОВ С СД 2 ТИПА

Аннотация

Частота возникновения неалкогольной жировой болезни печени (НАЖБП) быстро растет во всем мире, став в настоящее время самой распространенной патологией печени. Ее объединяет с патологиями, входящими в состав метаболического синдрома (висцеральное ожирение, дислипидемия, артериальная гипертензия и нарушения углеводного обмена) общая патогенетическая основа - инсулинрезистентность. С учетом высокой распространенности НАЖБП идентификация неинвазивных предикторов ее развития и, что особенно важно, ее прогрессии с развитием фиброза до цирроза, имеет ключевое значение. Уровень гормонов жировой ткани - адипоцитокинов, напрямую связан с выраженностью инсулинрезистентности и в высокой степени детерминирует процессы воспаления и фиброзирования в печени. Соответственно, данные гормоны являются хорошими кандидатами как на роль предикторов развития и прогрессии НАЖБП, так и на роль маркеров динамического контроля метаболических эффектов терапии. Гормоны, участвующие в регуляции пищевого поведения (лептин, грелин, глюкагоно-подобный пептид 1 типа) оказывают существенные эффекты на метаболизм жировой ткани и как ее чувствительность к инсулину, так и чувствительность к инсулину ткани печени. Их динамика в процессе терапии НАЖБП также может быть важным маркером ее эффективности. Данный обзор посвящен роли адипоцитокинов и некоторых других гормонов, участвующих в регуляции чувствительности тканей к инсулину, процессов воспаления и фиброза в предикции развития, прогрессирования и ответе на терапию НАЖБП.

Об авторах

А. Ю. Бабенко
«Национальный медицинский исследовательский центр им. В. А. Алмазова» Министерства Здравоохранения России
Россия


А. Г. Архипова
«Национальный медицинский исследовательский центр им. В. А. Алмазова» Министерства Здравоохранения России
Россия


В. К. Байрашева
«Национальный медицинский исследовательский центр им. В. А. Алмазова» Министерства Здравоохранения России
Россия


Е. В. Шляхто
«Национальный медицинский исследовательский центр им. В. А. Алмазова» Министерства Здравоохранения России
Россия


Список литературы

1. Bedogni G., Miglioli L., Masutti F. et al. Prevalence of and risk factors for nonal-coholic fatty liver disease: The Dionysos Nutrition and Liver Study. Hepatology, 2005, vol. 4, pp. 44-52.

2. Drapkina O.M., Ivashkin V. T. Epidemiological features of nonalcoholic fatty liver disease in Russia (the results of an open, multicentre prospective observational study DIREGL 01903). Russian Journal gastroenterology, Hepatology, coloproctology, 2014, vol. 24, no. 4, pp. 32-38.

3. Vanni E., Bugianesi E., Kotronen A. et al. From the metabolic syndrome to NAFLD or vice versa? Dig Liver Dis, 2010, vol. 42, pp. 320-330.

4. Bataller R., Rombouts K., Altamirano J., Marra F. Fibrosis in alcoholic and nonal-coholic steatohepatitis. Best Pract Res Clin Gastroenterol, 2011, vol. 25, pp. 231-244.

5. Неалкогольная жировая болезнь печени: клиника, диагностика, лечение / Л. Б. Лазебник и соавт. // Экспериментальная и клиническая гастроэнтерология. 2015;119(7):85-96.

6. Cheah M.C.C., McCullough A.J., Goh G. B. B. Current modalities of fibrosis assessment in nonalcoholic fatty liver disease. J Clin Transl Hepatol, 2017, vol.5, no. 3, pp. 261-271.

7. Селивёрстов П.В. Неалкогольная жировая болезнь печени: от теории к практике // Архив внутренней медицины. 2015. № 1 (21). С. 19-26.

8. Селивёрстов П. В. Ожирение как фактор риска развития сердечно-сосудистых осложнений на фоне неалкогольной жировой болезни печени. Медицинский альманах. 2016;1(41):61-3.

9. NICE guideline Non-alcoholic fatty liver disease. National Institute for Health and Care Excellence, 2016, pp. 51-65.

10. Chang Y., Jung H. S., Cho J., et al. Metabolically Healthy Obesity and the Development of Nonalcoholic Fatty Liver Disease. Am J Gastroenterol, 2016, vol. 111, no. 8, pp. 1133-1140.

11. Caballería L.l., Auladell A. M., Torán P., et al. Prevalence and factors associated with the presence of non alcoholic fatty liver disease in an apparently healthy adult population in primary care units. BMC Gastroenterology, 2007, vol. 7, p. 41.

12. Machado M.V., Coutinho J., Carepa F., et al. How adiponectin, leptin, and ghrelin orchestrate together and correlate with the severity of nonalcoholic fatty liver disease. Eur J Gastroenterol Hepatol, 2012, vol. 24, no. 10, pp. 1166-1172.

13. Dixon J.B., Bhatal P. S., O’Brien P. E. Nonalcoholic fatty liver disease: Predictors of nonalcoholic steatohepatitis and liver fibrosis in the severity obese. Gastroenterology, 2001, vol. 121, pp. 91-100.

14. Stranges S., Dorn J. M., Muti P., et al. Body fat distribution, relative weight, and liver enzyme levels: a population-based study. Hepatology, 2004, vol. 39, pp. 754-763.

15. Abd El-Kader S.M., El-Den Ashmawy E. M. Non-alcoholic fatty liver disease: The diagnosis and management. World J Hepatol, 2015, vol. 7, no. 6, pp. 846-858.

16. Pappachan J.M., Antonio F. A., Edavalath M., Mukherjee A. Non-alcoholic fatty liver disease: a diabetologist’s perspective. Endocrine, 2014, vol. 45, pp. 344-353.

17. The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology, 2012, vol. 142, pp. 1592-1609.

18. Gentile C.L., Weir T. L., Cox-York K.A., et al. The role of visceral and subcutaneous adipose tissue fatty acid composition in liver pathophysiology associated with NAFLD. Adipocyte, 2015, vol. 4, no. 2, pp. 101-112.

19. Foster M.T., Pagliassotti M. J. Metabolic alterations following visceral fat removal and expansion. Adipocyte, 2012, vol. 1, no. 4, pp. 192-199.

20. Bugianesi E., Pagotto U., Manini R., et al. Plasma adiponectin in nonalcoholic fatty liver is related to hepatic insulin resistance and hepatic fat content, not to liver disease severity. J Clin Endocrinol Metab, 2005, vol. 90, pp. 3498-3504.

21. Polyzos S.A., Aronis K. N., Kountouras J., et al. Circulating leptin in non-alcoholic fatty liver disease: a systematic review and meta-analysis. Diabetologia, 2016, vol. 59, pp. 30-43.

22. Petta S., Gastaldelli A., Rebelos E., et al. Pathophysiology of non alcoholic fatty liver disease. Int J Mol Sci, 2016, vol. 1712, p. 2082.

23. Dixon J.B., Bhathal P. S., O’brien P. E. Nonalcoholic Fatty Liver Disease: Predic-tors of Nonalcoholic Steatohepatitis and Liver Fibrosis in the Severely Obese. Gastroenterology, 2001, vol. 121, pp. 91-100.

24. Mollard R.C., Senechal M., Macintosh A. C., et al. Dietary determinants of hepatic steatosis and visceral adiposity in overweight and obese youth at risk of type 2 dia-betes. Am J Clin Nutr, 2014, vol. 99, pp. 804-812.

25. Gentile C.L., Nivala A. M., Gonzales J. C., et al. Experimental evidence for therapeutic potential of taurine in the treatment of nonalcoholic fatty liver disease. Am J Physiol Regul Integr Comp Physiol, 2011, vol. 301, pp. 1710-1722.

26. Sattar N., Gaw A., Scherbakova O. et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation, 2003, vol. 108, pp. 414-419.

27. Fallo F., Scarda A., Sonino N. et al. Effect of glucocorticoids on adiponectin: a study in healthy subjects and in Cushing´s syndrome. Eur. J. Endocrinol, 2004, vol. 150, pp. 339-344.

28. Mohlig M., Wegewitz U., Osterhoff M. et al. Insulin decreases human adiponectin plasma levels. Horm Metab Res, 2002, vol. 34, pp. 655-658.

29. Delporte M. L., Funahashi T., Takahashi M. et al. Pre- and post-translational negative effect of badrenoreceptor agonists on adiponectin secretion: in vitro and in vivo studies. Biochem J, 2002, vol. 367, pp. 677-685.

30. Yang W. S., Jeng C. Y., Wu T. J. et al. Synthetic peroxisome proliferator-activated receptor gamma agonist, rosiglitazone, increases plasma levels of adiponectin in type 2 diabetic patients. Diabetes Care, 2002, vol. 25, pp. 376-380.

31. Maeda N., Takahashi M., Funahashi T. et al. PPAR gamma ligands increase expression and plasma concentrations of adiponectin an adipose derived protein. Diabetes, 2001, vol. 50, pp. 2094-2099.

32. Lopaschuk G. D., Ussher J. R., Folmes C. D. L. et al. Myocardial Fatty Acid Metabolism in Health and Disease. Physiol. Rev, 2010, vol. 90, pp. 207-258.

33. Buechler C., Haberl E. M., Rein-Fischboeck L., Aslanidis C. Adipokines in Liver Cirrhosis. Int J Mol Sci, 2017, vol. 18, no.7, p. 1392.

34. Koehler E., Swain J., Sanderson S., et al. Growth hormone, dehydroepiandrosterone and adiponectin levels in non-alcoholic steatohepatitis: an endocrine signature for advanced fibrosis in obese patients. Liver Int, 2012, vol. 32, pp. 279-286.

35. Correnti J.M., Cook D., Aksamitiene E., et al. Adiponectin fine-tuning of liver regeneration dynamics revealed through cellular network modelling. J Physiol, 2015, vol. 593, pp. 365-383.

36. Savvidou S., Hytiroglou P., Orfanou-Koumerkeridou H. et al. Low serum adi-ponectin levels are predictive of advanced hepatic fibrosis in patients with NAFLD. J Clin Gastroenterol, 2009, vol. 43, no. 8, pp. 765-772.

37. Shimada M., Kawahara H., Ozaki K., et al. Usefulness of a combined evaluation of the serum adiponectin level, HOMA-IR, and serum type IV collagen 7S level to predict the early stage of nonalcoholic steatohepatitis. Am J Gastroenterol, 2007, vol. 102, no. 9, pp. 1931-1938.

38. Biddinger S.B., Miyazaki M., Boucher J. et al. Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of insulin and sterol regulatory element-binding protein-1c. Diabetes. 2006, vol. 55, pp. 2032-2041.

39. Koerner A., Kratzsch J., Kiess W. Adipocytokines: leptin - the classical, resistin - the controversical, adiponectin - the promising, and more to come. Best. Pract. Res. Clin. Endocrinol. Metab, 2005, vol. 19, pp. 525-546.

40. Haas V., Onur S., Paul T. et al. Leptin and body weight regulation in patients with anorexia nervosa before and during weight recovery. Am. J. Clin. Nutr, 2005, vol. 81, no.4, pp. 889-896.

41. Singh P., Peterson T. E., Sert-Kuniyoshi F. H. et al. Leptin signaling in adipose tissue: role in lipid accumulation and weight gain. Circ. Res, 2012, vol.111. no. 5, pp. 599-603.

42. Chitturi S., Farrell G., Frost L. et al. Serum leptin in NASH correlates with hepatic steatosis but not fibrosis: a manifestation of lipotoxicity? Hepatology, 2002, vol. 36, pp. 403-409.

43. Huang X.D., Fan Y., Zhang H. et al. Serum leptin and soluble leptin receptor in non-alcoholic fatty liver disease. World J Gastroenterol, 2008, vol. 14, pp. 2888-2893.

44. Wang J., Leclercq I., Brymora J. M. et al. Kupffer cells mediate leptin-induced liver fibrosis. Gastroenterology, 2009, vol. 137, pp. 713-723.

45. Bugianesi E., Pagotto U., Manini R. et al. Plasma adiponectin in nonalcoholic fatty liver is related to hepatic insulin resistance and hepatic fat content, not to liver disease severity. J Clin Endocrinol Metab, 2005, vol. 90, pp. 3498-3504.

46. Krecki R., Krzeminska-Pakula M., Peruga J. Z. et al. Elevated resistin opposed to adiponectin or angiogenin plasma levels as a strong, independent predictive factor for the occurrence of major adverse cardiac and cerebrovascular events in patients with stable multivessel coronary artery disease over 1-year follow-up. Med. Sci. Monit, 2011, vol. 17, no.1, pp. CR26-CR32.

47. Reilly M. P., Lehrke M., Wolfe M. L. et al. Resistin is an inflammatory marker of atherosclerosis in humans. Circulation, 2005, vol. 111, no.7, pp. 932-939.

48. Jung H. S., Park K. H., Cho Y. M. et al. Resistin is secreted from macrophages in atheromas and promotes atherosclerosis. Cardiovasc. Res., 2006, vol. 69, no. 1, pp. 76-85.

49. Verma S., Li S. H., Wang C. H. et al. Resistin promotes endothelial cell activation: further evidence of adipokine-endothelial interaction. Circulation, 2003, vol. 108, no. 6, pp. 736-740.

50. Vendrell J., Broch M., Vilarrasa N. et al. Resistin, adiponectin, ghrelin, leptin, and proinflammatory cytokines: relationships in obesity. Obes. Res. 2004, vol. 12, no. 6, pp. 962-971.

51. Bokarewa M., Nagaev I., Dahlberg L. et al. Resistin, an adipokine with potent proinflammatory properties. J. Immunol. 2005, vol. 174, no. 9, pp. 5789-5795.

52. Rajala M. W., Obici S., Scherer P. E. et al. Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production. J. Clin. Invest. 2003, vol. 111, no. 2, pp. 225-230.

53. Emanuelli B., Peraldi P., Filloux C. et al. SOCS-3 inhibits insulin signaling and is up-regulated in response to tumor necrosis factor-a in the adipose tissue of obese mice. Journal of Biological Chemistry, 2001, vol. 276, pp. 47944-47949.

54. Fujinami A., Obayashi H., Ohta K. et al. Enzyme-linked immunosorbent assay for circulating human resistin: resistin concentrations in normal subjects and patients with type 2 diabetes. Clin. Chim. Acta, 2004, vol. 339, no. 1, pp. 57-63.

55. Pagano C., Soardo G., Pilon C. et al. Increased serum resistin in nonalcoholic fat-ty liver disease is related to liver disease severity and not to insulin resistance. J Clin Endocrinol Metab, 2006, vol. 91, pp. 1081-1086.

56. Aller R., de Luis D. A., Izaola O. et al. Influence of visfatin on histopathological changes of non-alcoholic fatty liver disease. Dig Dis Sci, 2009, vol. 54, pp. 1772-1777.

57. Yilmaz Y., Yonal O., Kurt R. et al. Serum levels of omentin, chemerin and adipsin in patients with biopsy-proven nonalcoholic fatty liver disease. Scand J Gastroenterol, 2011, vol. 46, pp. 91-97.

58. Newcomer M. E., Ong D. E. Plasma retinol binding protein: structure and function of the prototypic lipocalin. Biochimica et Biophysica Acta, 2000, vol. 1482, pp. 57-64.

59. Kos K., Wong S., Tan B. et al. Human RBP4 adipose tissue expression is gender specific and influenced by leptin. Clinical Endocrinology, 2010. vol. 74, pp. 197-205.

60. Sell H., Eckel J. Regulation of retinol binding protein 4 production in primary human adipocytes by adiponectin, troglitazone and TNF-alpha. Diabetologia, 2007, vol. 50, pp. 2221-2223.

61. Qi Q., Yu Z., Ye X. et al. Elevated retinol binding protein-4 levels are associated with metabolic syndrome in Chinese people. J. Clin. Endocrin. Metab, 2007, vol. 92, pp. 4827-4834.

62. Fernandez-Real J. M., Moreno J. M., Ricart W. Circulating retinolbinding protein-4 concentration might reflect insulin resistance-associated iron overload. Diabetes, 2008, vol. 57, pp. 1918-1925.

63. Erikstrup C., Mortensen O. H., Nielsen A. R. et al. RBP-to-retinol ratio, but not total RBP, is elevated in patients with type 2 diabetes. Diabetes, Obesity &Metabolism. 2009, vol. 11, pp. 204-212.

64. Zugaro A., Pandolfi C., Barbonetti A. et al. Retinol binding protein 4, low birth weight-related insulin resistance and hormonal contraception. Endocrine, 2007, vol. 32, pp. 166-169.

65. Mallat Z., Simon T., Benessiano J. et al. Retinol-binding protein 4 and prediction of incident coronary events in healthy men and women. Journal of Clinical Endocrinology and Metabolism, 2009, vol. 94, pp. 255-260.

66. Kadowaki T., Yamauchi T., Kubota N. et al. Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome. J. Clin. Invest, 2006, vol. 116, no.7, pp. 1784-1792.

67. Asaoka Y., Terai S, Sakaida I., Nishina H. The expanding role of fish models in understanding non-alcoholic fatty liver disease. Dis Model Mech, 2013, vol. 6, pp. 905-914.

68. Stefan N., Kantartzis K., Häring H. U. Causes and metabolic consequences of Fatty liver. Endocr Rev, 2008, vol. 29, pp. 939-960.

69. Loria P., Lonardo A., Anania F. Liver and diabetes. A vicious circle. Hepatol Res, 2013, vol. 43, pp. 51-64.

70. Foster-Schubert K. E., Overduin J., Prudom C. E. et al. Acyl and total ghrelin are suppressed strongly by ingested proteins, weakly by lipids, and biphasically by carbohydrates. Journal of Clinical Endocrinology and Metabolism, 2008, vol. 93, pp. 1971-1979.

71. Lawrence C. B., Snape A. C., Baudoin F. M. et al. Acute central ghrelin and GH secretagogues induce feeding and activate brain appetite centres. Endocrinology, 2002, vol. 143, pp. 155-162.

72. Date Y., Kojima M., Hosoda H. et al. Ghrelin, a novel growth hormone-releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tracts of rats and humans. Endocrinology, 2000, vol. 141, pp. 4255-4261.

73. Arvat E., Maccario M., Di Vitro L. et al. Endocrine activities of ghrelin, a natural growth hormone secretagogue (GHS), in humans: comparison and interactions with hexarelin, a nonnatural peptidyl GHS, and GH-releasing hormone. J. Clin. Endocrin. Met, 2001, vol. 86, pp. 1169-1174.

74. Theander-Carrillo C., Wiedmer P., Cettour-Rose P. et al. Ghrelin action in brain controls adipocyne metabolism. J Clin Invest, 2006, vol. 116, pp. 1983-1993.

75. Cowley M. A. The distribution and mechanism of action of ghrelin in the CNS demonstrates a novel hypothalamic circuit regulating energy homeostasis. Neuron, 2003, vol. 37, pp. 649-661.

76. Waseem T., Duxbury M., Ito H. et al. Exogenous ghrelin modulates release of pro-inflammatory cytokones in LPS-stimulated macrophages through distinct signalling pathways. Surgery, 2008, vol. 143, pp. 334-342.

77. Machado M.V., Coutinho J., Carepa F. et al. How adiponectin, leptin, and ghrelin orchestrate together and correlate with the severity of nonalcoholic fatty liver disease. Eur J Gastroenterol Hepatol, 2012, vol. 24, no. 10, pp. 166-172.

78. Blom W. A., Stafleu A., de Graaf C. et al. Ghrelin response to carbohydrate-enriched breakfast is related to insulin. Am. J. Clin. Nutr, 2005, vol. 81, pp. 367-375.

79. Hou X., Xu S., Maitland-Toolan K. A. et al. SIRT1 regulates hepatocyte lipid me-tabolism through activating AMP-activated protein kinase. J Biol Chem, 2008, vol. 283, pp. 20015-20026.

80. Bernsmeier C., Meyer-Gerspach A.C., Blaser L. S. et al. Glucose-induced gluca-gon-like Peptide 1 secretion is deficient in patients with non-alcoholic fatty liver dis-ease. PLoS One. 2014, p. 9: e87488

81. Firneisz G., Varga T., Lengyel G. et al. Serum dipeptidyl peptidase-4 activity in insulin resistant patients with non-alcoholic fatty liver disease: a novel liver disease biomarker. PLoS One. 2010, p. 5: e12226

82. Svegliati-Baroni G., Saccomanno S., Rychlicki C. et al. Glucagon-like peptide-1 receptor activation stimulates hepatic lipid oxidation and restores hepatic signalling alteration induced by a high-fat diet in nonalcoholic steatohepatitis. Liver Int. 2011, vol. 31, pp. 1285-1297.

83. Cusi K. Role of obesity and lipotoxicity in the development of nonalcoholic steatohepatitis: pathophysiology and clinical implications. Gastroenterology, 2012, vol. 142, pp. 711-725.

84. Portillo-Sanchez1 P., Cus K. Treatment of Nonalcoholic Fatty Liver Disease (NAFLD) in patients with Type 2 Diabetes Mellitus. Clin Diabetes Endocrinol, 2016, vol. 2, p. 9.

85. Promrat K., Kleiner D. E., Niemeier H. M. Randomized controlled trial testing the effects of weight loss on nonalcoholic steatohepatitis. Hepatology, 2010, vol. 51, pp. 121-129.

86. Arias-Loste MT, Ranchal I, Romero-Gómez M, Crespo J. Irisin, a link among fatty liver disease, physical inactivity and insulin resistance. Int J Mol Sci. 2014;15:23163-23178. 10.3390/ijms151223163.

87. Mann T., Tomiyama A. J., Westling E. et al. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol, 2007, vol. 62, no. 3, pp. 220-233.

88. Schwartz A., Doucet E. Relative changes in resting energy expenditure during weight loss: a systematic review. Obes Rev, 2010, vol. 11, no. 7, pp. 531-547.

89. Sumithran p., Prendergast L. A., DelbridgeE. et al. Long-Term Persistence of Hormonal Adaptations to Weight Loss. N Engl J Med, 2011, vol. 365, pp. 1597-1604.

90. Бабенко А.Ю., Тихоненко Е. В. и соавт. Ожирение и метаболизм (в печати) Crujeiras A.B., Goyenechea E., Abete I. et al. Weight regain after a diet-induced loss is predicted by higher baseline leptin and lower ghrelin plasma levels. Journal Of Clinical Endocrinology And Metabolism, 2010, vol. 95, no. 11, pp. 5037-5044.

91. Barb D., Portillo-Sanchez P., Cusi K. Pharmacological management of nonalcoholic fatty liver disease. Metabolism: Clinical and Experimental, 2016, vol. 65, pp. 1183-1195.

92. Abdul-Ghani M., DeFronzo R. A. Is It Time to Change the Type 2 Diabetes Treatment Paradigm? Yes! GLP-1 ras Should Replace Metformin in the Type 2 Dia-betes Algorithm. Diabetes Care, 2017, vol. 40, pp. 1121-1127.

93. Pappachan J.M., Babu S., Krishnan B., Ravindran M. Non-alcoholic fatty liver disease: a clinical update. J Clin Transl Hepatol, 2017, vol. 5, no. 4, pp. 384-393.

94. Harrison S.A., Fecht W., Brunt E. M., Neuschwander-Tetri B. A. Orlistat for overweight subjects with nonalcoholic steatohepatitis: a randomized, prospective trial. Hepatology, 2009, vol. 49, no.1, pp. 80-86.

95. Musso G., Gambino R., Cassader M., Pagano G. A meta-analysis of randomized trials for the treatment of nonalcoholic fatty liver disease. Hepatology, 2010, vol. 52, pp. 79-104.

96. Ratziu V., Caldwell S., Neuschwander-Tetri B. A. Therapeutic trials in nonalcoholic steatohepatitis: insulin sensitizers and related methodological issues. Hepatolo-gy, 2010, vol. 52, pp. 2206-2215.

97. Loomba R., Lutchman G., Kleiner D. E. et al. Clinical trial: pilot study of metformin for the treatment of non-alcoholic steatohepatitis. Aliment Pharmacol Ther, 2009, vol. 29, pp. 172-182.

98. Kim S., Ohta K., Hamaguchi A. et al. Angiotensin II type I receptor antagonist inhibits the gene expression of transforming growth factor-beta 1 and extracellular matrix in cardiac and vascular tissues of hypertensive rats. J Pharmacol Exp Ther, 1995, vol. 273, pp. 509-515.

99. Friedman S. L. Cytokines and fibrogenesis. Semin Liver Dis, 1999, vol. 19, pp. 129-140.

100. Yokohama S., Yoneda M., Haneda M., et al. Therapeutic efficacy of an angiotensin II receptor antagonist in patients with nonalcoholic steatohepatitis. Hepatology, 2004, vol. 40, no.5, pp. 1222-1225.

101. Watanabe S., Hashimoto E., Ikejima K. et al. Evidence-based clinical practice guidelines for nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. J Gastroenterol, 2015, vol. 50, no. 4, 364-377.

102. Pawlak M., Lefebvre P., Staels B. Molecular mechanism of PPARalpha action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. J Hepatol, 2015, vol. 62, no. 3, pp. 720-733.

103. Fabbrini E., Mohammed B. S., Korenblat K. M., et al. Effect of fenofibrate and niacin on intrahepatic triglyceride content, very low-density lipoprotein kinetics, and insulin action in obese subjects with nonalcoholic fatty liver disease. J Clin Endocrinol Metab, 2010, vol. 95, no.6, pp. 2727-2735.

104. Portillo-Sanchez P., Cusi K. Treatment of Nonalcoholic Fatty Liver Disease (NAFLD) in patients with Type 2 Diabetes Mellitus. Clin Diabetes Endocrinol, 2016, vol. 2, pp. 9.

105. Bhat A., Sebastiani G., Bhat M. Systematic review: Preventive and therapeutic applications of metformin in liver disease. World J Hepatol, 2015, vol. 7, pp. 1652-1659.

106. Sanyal A.J., Chalasani N., Kowdley K. V., et al. Pioglitazone, vitamin E, or pla-cebo for nonalcoholic steatohepatitis. N Engl J Med, 2010, vol. 362, pp. 1675-85.

107. Cusi K., Orsak B., Lomonaco R., et al. Extended treatment with pioglitazone improves liver histology in patients with prediabetes or type 2 diabetes mellitus and NASH. Hepatology, 2013, vol. 58, Abstract #82.

108. Oz O., Tuncel E., Eryilmaz S. et al. Arterial elasticity and plasma levels of adi-ponectin and leptin in type 2 diabetic patients treated with thiazolidinediones. Endocr, 2008, vol. 33, pp.101-105.

109. Combs T. P., Wagner J. A., Berger J. et al. Induction of adipocyte complement related protein of 30 kilodaltons by PPAR gamma agonists: a potential mechanism of insulin sensitization. Endocrinology, 2002, vol. 143, pp. 998-1007.

110. Kishore P., Li W. J., Weaver C., et al. Rapid in vivo Effects of Pioglitazone on Adipose Tissue Gene Expression and Insulin Action in Humans with Type 2 Diabetes Mellitus(T2DM)

111. Ding X., Saxena N. K., Lin S., et al. Exendin-4, a glucagon-like protein-1 (GLP-1) receptor agonist, reverses hepatic steatosis in ob/ob mice. Hepatology, 2006, vol. 43, pp. 173-181.

112. Lee J., Hong S. W., Chae S. W. et al. Exendin-4 improves steatohepatitis by in-creasing sirt1 expression in high-fat diet-induced obese C57BL/6 J mice. PLoS One, 2012, vol. 7. p. e31394.

113. Trevaskis J.L., Griffin P. S., Wittmer C. et al. Glucagon-like peptide-1 receptor agonism improves metabolic, biochemical, and histopathological indices of nonalcoholic steatohepatitis in mice. Am J Physiol Gastrointest Liver Physiol, 2012, vol. 302, pp. G762-72.

114. Armstrong M.J., Houlihan D. D., Rowe I. A. et al. Safety and efficacy of liraglutide in patients with type 2 diabetes and elevated liver enzymes: individual patient data meta-analysis of the LEAD program. Aliment Pharmacol Ther, 2013, vol. 37, pp. 234-242.

115. Cuthbertson D.J., Irwin A, Gardner C. J. et al. Improved glycaemia correlates with liver fat reduction in obese, type 2 diabetes, patients given glucagon-like peptide-1 (GLP-1) receptor agonists. PLoS One, 2012, vol. 7. p. e50117.

116. Аrmstrong M.J., Gaunt P., Aithal G. P. et al. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, ran-domised, placebo-controlled phase 2 study. Lancet, 2016, vol. 387, pp. 679-90.

117. Тихоненко Е.В., Бабенко А. Ю. Предикторы ответа на терапию аГПП-1. В книге: Сахарный диабет - 2017: от мониторинга к управлению. Материалы II Российской мультидисплинарной конференции с международным участием. 2017.С.17-21

118. Clemmensen C, Chabenne J, Finan B. et al. GLP-1/glucagon coagonism restores leptin responsiveness in obese mice chronically maintained on an obesogenic diet. Diabetes. 2014;63:1422-1427.

119. Iepsen EW, Lundgren J, Dirksen C. et al. Treatment with a GLP-1 receptor agonist diminishes the decrease in free plasma leptin during maintenance of weight loss. International Journal of Obesity (London). 2015;39(5):834-841. doi: 10.1038/ijo.2014.177.

120. Moretto M., Kupski C., da Silva V. D. et al. Effect of bariatric surgery on liver fibrosis. Obes Surg, 2012, vol. 22, pp. 1044-1049.

121. de Almeida S. R., Rocha P. R., Sanches M. D. et al. Rouxen Y gastric bypass improves the nonalcoholic steatohepatitis (NASH) of morbid obesity. Obes Surg, 2006, vol. 16, pp. 270-278.

122. Tokito A., Koriyama N., Ijuin A. et al. Switching from Sitagliptin To Alogliptin under Treatment with Pioglitazone Increases High Molecular Weight Adiponectin in Type 2 Diabetes: A Prospective Observational Study. Journal of Diabetes Mellitus, 2015, vol. 5, pp. 258-266.

123. Polidori D., Sha S., Mudaliar S. et al. Canagliflozin lowers postprandial glucose and insulin by delaying intestinal glucose absorption in addition to increasing urinary glucose excretion: results of a randomized, placebo-controlled study. Diabetes Care, 2013, vol. 36, no.8, pp. 2154-2161.

124. Takebayashi K., Hara K., Terasawa T. et al. Effect of canagliflozin on circulating active GLP-1 levels in patients with type 2 diabetes: a randomized trial. Endocr J, 2017, vol. 64, no. 9, pp. 923-931.

125. Ferrannini E., Muscelli E., Frascerra S. et al. Metabolic response to sodium-glucose cotransporter 2 inhibition in type 2 diabetic patients. J Clin Invest, 2014, vol. 124, vol. 2, pp. 499-508.


Рецензия

Для цитирования:


Бабенко А.Ю., Архипова А.Г., Байрашева В.К., Шляхто Е.В. РОЛЬ АДИПОЦИТОКИНОВ, ГРЕЛИНА И ИНКРЕТИНОВ В ПРЕДИКЦИИ НЕАЛКОГОЛЬНОЙ ЖИРОВОЙ БОЛЕЗНИ ПЕЧЕНИ И ЕЕ ЛЕЧЕНИИ У ПАЦИЕНТОВ С СД 2 ТИПА. Экспериментальная и клиническая гастроэнтерология. 2018;(2):121-136.

For citation:


Babenko A.Yu., Arhipova A.G., Bayrasheva V.K., Shlyakhto E.V. ROLE OF ADIPOCYTOKINES, GHRELIN AND INCRETINS IN PREDICATION OF NON-ALCOHOLIC FATTY LIVER DISEASE AND ITS TREATMENT IN PATIENTS WITH TYPE 2 DIABETES. Experimental and Clinical Gastroenterology. 2018;(2):121-136. (In Russ.)

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