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Холецистэктомия как фактор риска прогрессирования неалкогольной жировой болезни печени
Холецистэктомия как фактор риска прогрессирования неалкогольной жировой болезни печени
Буеверов А.О. Холецистэктомия как фактор риска прогрессирования неалкогольной жировой болезни печени. Consilium Medicum. 2019; 21 (8): 93–97. DOI: 10.26442/20751753.2019.8.190503
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Аннотация
Взаимосвязь неалкогольной жировой болезни печени (НАЖБП), желчнокаменной болезни (ЖКБ) и холецистэктомии (ХЭ) служит предметом исследования биохимиков, патофизиологов, морфологов, клиницистов. Взаимная ассоциация ЖКБ и НАЖБП реализуется в первую очередь посредством инсулинорезистентности. Однако в последние годы появились убедительные данные о том, что не только и не столько ЖКБ, сколько ХЭ играет важную роль в прогрессировании НАЖБП. Это обусловлено нарушением эндокринного баланса и сигнальной функции желчных кислот, а также развитием синдрома избыточного бактериального роста в тонкой кишке. Дальнейшее изучение этих взаимоотношений не только позволяет воздержаться от необоснованных оперативных вмешательств, но и открывает перспективы разработки новых методов лечения. Урсодезоксихолевая кислота (Урсосан) может быть применена у таких пациентов с двойной целью – воздействие на патогенетические механизмы НАЖБП и уменьшение литогенности желчи.
Ключевые слова: неалкогольная жировая болезнь печени, желчнокаменная болезнь, холецистэктомия, патогенез.
Ключевые слова: неалкогольная жировая болезнь печени, желчнокаменная болезнь, холецистэктомия, патогенез.
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Association between non-alcoholic fatty liver disease (NAFLD), cholelithiasis, and cholecystectomy is a research subject for biochemists, pathophysiologists, morphologists and clinical physicians. Association between cholelithiasis and NAFLD is mostly presented by insulin resistance. Although in present years solid evidence have emerged showing that not so much cholelithiasis as cholecystectomy has an important role in NAFLD progression. It is determined by endocrine balance and bile acids signal function disturbance as well as by small bowel bacterial overgrowth syndrome development. Further study of these interrelations not only will allow holding from unreasonable surgeries, but will also offer perspectives for development of new treatment methods.
Key words: non-alcoholic fatty liver disease, cholelithiasis, cholecystectomy, pathogenesis.
Key words: non-alcoholic fatty liver disease, cholelithiasis, cholecystectomy, pathogenesis.
Полный текст
Список литературы
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[Samsonov A.A., Plotnikova E.Iu., Ruban A.P. et al. Zhelchnokamennaia bolezn', kholetsistektomiia – chto dal'she? Med. sovet. 2014; 4: 50–4 (in Russian).]
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[Lebedeva O.V., Bueverov A.O., Bueverova E.L., Nikitina L.O. Vliianie kholetsistektomii v molodom vozraste na techenie metabolicheskogo sindroma u zhenshchin. Al'manakh klin. med. 2017; 45 (6): 326–33 (in Russian).]
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41. Yun S, Choi D, Lee KG et al. Cholecystectomy causes ultrasound evidence of increased hepatic steatosis. World J Surg 2016; 40: 1412–21.
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46. Guo L, Mao J, Li Y et al. Cholelithiasis, cholecystectomy and risk of hepatocellular carcinoma: a meta-analysis. J Cancer Res Ther 2014; 10 (4): 834–8.
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48. Ratziu V, de Ledinghen V, Oberti F et al. A randomized controlled trial of high-dose ursodesoxycholic acid for nonalcoholic steatohepatitis. J Hepatol 2011; 54 (5): 1011–9.
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51. Stokes CS, Gluud LL, Casper M, Lammert F. Ursodeoxycholic acid and diets higher in fat prevent gallbladder stones during weight loss: a meta-analysis of randomized controlled trials. Clin Gastroenterol Hepatol 2014; 12 (7): 1090–100.
2. Estes C, Anstee QM, Arias-Loste MT. Modeling NAFLD burden in China, France, Germany, Italy, Japan, Spain, United Kingdom, and United States for the period 2016–2030. J Hepatol 2018. pii: S0168-8278(18)32121–32124.
3. Li AA, Ahmed A, Kim D et al. Extrahepatic manifestations of nonalcoholic fatty liver disease. Gut Liver 2019. DOI: 10.5009/gnl19069.
4. Sayiner M, Koenig A, Henry L, Younossi ZM. Epidemiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in the United States and the rest of the world. Clin Liver Dis 2016; 20: 205–14.
5. Bellentani S. The epidemiology of nonalcoholic fatty liver disease. Liver Int 2017; 37 (Suppl. 1): 81–4.
6. EASL Clinical Practice Guidelines on the prevention, diagnosis and treatment of gallstones. J Hepatol 2016; 65: 146–81.
7. Mendez-Sanchez N, Bahena-Aponte J, Chavez-Tapia NC et al. Strong association between gallstones and cardiovascular disease. Am J Gastroenterol 2005; 100: 827–30.
8. Ahmed MH, Ali A. Nonalcoholic fatty liver disease and cholesterol gallstones: which comes first? Scand J Gastroenterol 2014; 49: 521–7.
9. Arrese M, Cortés V, Barrera F, Nervi F. Nonalcoholic fatty liver disease, cholesterol gallstones, and cholecystectomy: new insights on a complex relationship. Curr Opin Gastroenterol 2018; 34 (2): 90–6.
10. Samsonov A.A., Plotnikova E.Iu., Ruban A.P. et al. Zhelchnokamennaia bolezn', kholetsistektomiia – chto dal'she? Med. sovet. 2014; 4: 50–4 (in Russian).
11. Lammert F, Gurusamy K, Ko CW et al. Gallstones. Nat Rev Dis Primers 2016; 2: 16024.
12. Chiang JY. Bile acid metabolism and signaling. Comprehens Physiol 2013; 3: 1191–212.
13. Jaruvongvanich V, Sanguankeo A, Upala S. Significant association between gallstone disease and nonalcoholic fatty liver disease: a systematic review andmeta-analysis. Dig Dis Sci 2016; 61: 2389–96.
14. Housset C, Chretien Y, Debray D, Chignard N. Functions of the gallbladder. Comprehens Physiol 2016; 6: 1549–77.
15. Koller T, Kollerova J, Hlavaty T et al. Cholelithiasis and markers of nonalcoholic fatty liver disease in patients with metabolic risk factors. Scand J Gastroenterol 2012; 47: 197–203.
16. Cortes V, Quezada N, Uribe S et al. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in nonobese Hispanic patients: a pilot study. Lipids in health and disease 2017; 16: 129.
17. Chang Y, Noh YH, Suh BS et al. Bidirectional association between nonalcoholic fatty liver disease and gallstone disease: a cohort study. J Clin Med 2018; 7 (11). pii: E458.
18. Rosso C, Mezzabotta L, Gaggini M et al. Peripheral insulin resistance predicts liver damage in nondiabetic subjects with nonalcoholic fatty liver disease. Hepatology 2016; 63: 107–16.
19. Li S, Brown MS, Goldstein JL. Bifurcation of insulin signaling pathway in rat liver: mTORC1 required for stimulation of lipogenesis, but not inhibition of gluconeogenesis. Proc Natl Acad Sci USA 2010; 107: 3441–6.
20. Lambert JE, Ramos-Roman MA, Browning JD, Parks EJ. Increased de novo lipogenesis is a distinct characteristic of individuals with nonalcoholic fatty liver disease. Gastroenterology 2014; 146: 726–35.
21. Tanaka N, Aoyama T, Kimura S, Gonzalez FJ. Targeting nuclear receptors for the treatment of fatty liver disease. Pharmacol Ther 2017; 179: 142–57.
22. Arab JP, Karpen SJ, Dawson PA et al. Bile acids and nonalcoholic fatty liver disease: molecular insights and therapeutic perspectives. Hepatology 2017; 65: 350–62.
23. Amigo L, Husche C, Zanlungo S et al. Cholecystectomy increases hepatic triglyceride content and very-low-density lipoproteins production in mice. Liver Int 2011; 31: 52–64.
24. Portincasa P, Di Ciaula A, Wang HH et al. Coordinate regulation of gallbladder motor function in the gut-liver axis. Hepatology 2008; 47: 2112–26.
25. Roda E, Aldini R, Mazzella G et al. Enterohepatic circulation of bile acids after cholecystectomy. Gut 1978; 19: 640–9.
26. Deutschmann K, Reich M, Klindt C et al. Bile acid receptors in the biliary tree: TGR5 in physiology and disease. Biochim Biophys Acta 2017.
27. Inagaki T, Choi M, Moschetta A et al. Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis. Cell Metab 2005; 2: 217–25.
28. Kliewer SA, Mangelsdorf DJ. Bile acids as hormones: the FXR-FGF15/19 pathway. Dig Dis 2015; 33: 327–31.
29. Barrera F, Azocar L, Molina H et al. Effect of cholecystectomy on bile acid synthesis and circulating levels of fibroblast growth factor 19. Ann Hepatol 2015; 14: 710–21.
30. Wojcik M, Janus D, Dolezal-Oltarzewska K et al. A decrease in fasting FGF19 levels is associated with the development of nonalcoholic fatty liver disease in obese adolescents. J Pediat Endocrinol Metab 2012; 25 (11–12): 1089–93.
31. Pols TW, Noriega LG, Nomura M et al. The bile acid membrane receptor TGR5: a valuable metabolic target. Dig Dis 2011; 29: 37–44.
32. Keitel V, Haussinger D. Perspective: TGR5 (Gpbar-1) in liver physiology and disease. Clin Res Hepatol Gastroenterol 2012; 36: 412–19.
33. Thomas C, Gioiello A, Noriega L et al. TGR5-mediated bile acid sensing controls glucose homeostasis. Cell Metab 2009; 10: 167–77.
34. Jones SA. Physiology of FGF15/19. Adv Exp Med Biol 2012; 728: 171–82.
35. Matsubara T, Li F, Gonzalez FJ. FXR signaling in the enterohepatic system. Mol Cell Endocrinol 2013; 368 (1–2): 17–29.
36. Cortes V, Quezada N, Uribe S et al. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in nonobese Hispanic patients: a pilot study. Lipids in health and disease 2017; 16: 129.
37. Lebedeva O.V., Bueverov A.O., Bueverova E.L., Nikitina L.O. Vliianie kholetsistektomii v molodom vozraste na techenie metabolicheskogo sindroma u zhenshchin. Al'manakh klin. med. 2017; 45 (6): 326–33 (in Russian).
38. Ruhl CE, Everhart JE. Relationship of nonalcoholic fatty liver disease with cholecystectomy in the US population. Am J Gastroenterol 2013; 108: 952–8.
39. Ioannou GN. Cholelithiasis, cholecystectomy, and liver disease. Am J Gastroenterol 2010; 105: 1364–73.
40. Kwak MS, Kim D, Chung GE et al. Cholecystectomy is independently associated with nonalcoholic fatty liver disease in an Asian population. World J Gastroenterol 2015; 21: 6287–95.
41. Yun S, Choi D, Lee KG et al. Cholecystectomy causes ultrasound evidence of increased hepatic steatosis. World J Surg 2016; 40: 1412–21.
42. Nervi F, Arrese M. Cholecystectomy and NAFLD: does gallbladder removal have metabolic consequences? Am J Gastroenterol 2013; 108: 959–61.
43. Shen C, Wu X, Xu C et al. Association of cholecystectomy with metabolic syndrome in a Chinese population. PloS One 2014; 9: e88189.
44. Hajong R, Dhal MR, Naku N et al. Incidence of nonalcoholic fatty liver disease in patients undergoing laparoscopic cholecystectomy. J Family Med Prim Care 2018; 7 (6): 1375–8.
45. Khaw KBC, Choi RH, Kam JH et al. Interval increase in the prevalence of symptomatic cholelithiasis-associated non-alcoholic fatty liver disease over a ten-year period in an Asian population. Singapore Med J 2017; 58 (12): 703–7.
46. Guo L, Mao J, Li Y et al. Cholelithiasis, cholecystectomy and risk of hepatocellular carcinoma: a meta-analysis. J Cancer Res Ther 2014; 10 (4): 834–8.
47. Chen Y, Wu S, Tian Y et al. Cholecystectomy as a risk factor of metabolic syndrome: from epidemiologic clues to biochemical mechanisms. Lab Invest 2018; 98 (1): 7–14.
48. Ratziu V, de Ledinghen V, Oberti F et al. A randomized controlled trial of high-dose ursodesoxycholic acid for nonalcoholic steatohepatitis. J Hepatol 2011; 54 (5): 1011–9.
49. Leuschner UF, Lindenthal B, Herrmann G et al. NASH Study Group. High-dose ursodeoxycholic acid therapy for nonalcoholic steatohepatitis: a double-blind, randomized, placebo-controlled trial. Hepatology 2010; 52 (2): 472–9.
50. Xiang Z, Chen YP, Ma KF et al. The role of ursodeoxycholic acid in non-alcoholic steatohepatitis: a systematic review. BMC Gastroenterol 2013; 13: 140.
51. Stokes CS, Gluud LL, Casper M, Lammert F. Ursodeoxycholic acid and diets higher in fat prevent gallbladder stones during weight loss: a meta-analysis of randomized controlled trials. Clin Gastroenterol Hepatol 2014; 12 (7): 1090–100.
2. Estes C, Anstee QM, Arias-Loste MT. Modeling NAFLD burden in China, France, Germany, Italy, Japan, Spain, United Kingdom, and United States for the period 2016–2030. J Hepatol 2018. pii: S0168-8278(18)32121–32124.
3. Li AA, Ahmed A, Kim D et al. Extrahepatic manifestations of nonalcoholic fatty liver disease. Gut Liver 2019. DOI: 10.5009/gnl19069.
4. Sayiner M, Koenig A, Henry L, Younossi ZM. Epidemiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in the United States and the rest of the world. Clin Liver Dis 2016; 20: 205–14.
5. Bellentani S. The epidemiology of nonalcoholic fatty liver disease. Liver Int 2017; 37 (Suppl. 1): 81–4.
6. EASL Clinical Practice Guidelines on the prevention, diagnosis and treatment of gallstones. J Hepatol 2016; 65: 146–81.
7. Mendez-Sanchez N, Bahena-Aponte J, Chavez-Tapia NC et al. Strong association between gallstones and cardiovascular disease. Am J Gastroenterol 2005; 100: 827–30.
8. Ahmed MH, Ali A. Nonalcoholic fatty liver disease and cholesterol gallstones: which comes first? Scand J Gastroenterol 2014; 49: 521–7.
9. Arrese M, Cortés V, Barrera F, Nervi F. Nonalcoholic fatty liver disease, cholesterol gallstones, and cholecystectomy: new insights on a complex relationship. Curr Opin Gastroenterol 2018; 34 (2): 90–6.
10. Самсонов А.А., Плотникова Е.Ю., Рубан А.П. и др. Желчнокаменная болезнь, холецистэктомия – что дальше? Мед. совет. 2014; 4: 50–4.
[Samsonov A.A., Plotnikova E.Iu., Ruban A.P. et al. Zhelchnokamennaia bolezn', kholetsistektomiia – chto dal'she? Med. sovet. 2014; 4: 50–4 (in Russian).]
11. Lammert F, Gurusamy K, Ko CW et al. Gallstones. Nat Rev Dis Primers 2016; 2: 16024.
12. Chiang JY. Bile acid metabolism and signaling. Comprehens Physiol 2013; 3: 1191–212.
13. Jaruvongvanich V, Sanguankeo A, Upala S. Significant association between gallstone disease and nonalcoholic fatty liver disease: a systematic review andmeta-analysis. Dig Dis Sci 2016; 61: 2389–96.
14. Housset C, Chretien Y, Debray D, Chignard N. Functions of the gallbladder. Comprehens Physiol 2016; 6: 1549–77.
15. Koller T, Kollerova J, Hlavaty T et al. Cholelithiasis and markers of nonalcoholic fatty liver disease in patients with metabolic risk factors. Scand J Gastroenterol 2012; 47: 197–203.
16. Cortes V, Quezada N, Uribe S et al. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in nonobese Hispanic patients: a pilot study. Lipids in health and disease 2017; 16: 129.
17. Chang Y, Noh YH, Suh BS et al. Bidirectional association between nonalcoholic fatty liver disease and gallstone disease: a cohort study. J Clin Med 2018; 7 (11). pii: E458.
18. Rosso C, Mezzabotta L, Gaggini M et al. Peripheral insulin resistance predicts liver damage in nondiabetic subjects with nonalcoholic fatty liver disease. Hepatology 2016; 63: 107–16.
19. Li S, Brown MS, Goldstein JL. Bifurcation of insulin signaling pathway in rat liver: mTORC1 required for stimulation of lipogenesis, but not inhibition of gluconeogenesis. Proc Natl Acad Sci USA 2010; 107: 3441–6.
20. Lambert JE, Ramos-Roman MA, Browning JD, Parks EJ. Increased de novo lipogenesis is a distinct characteristic of individuals with nonalcoholic fatty liver disease. Gastroenterology 2014; 146: 726–35.
21. Tanaka N, Aoyama T, Kimura S, Gonzalez FJ. Targeting nuclear receptors for the treatment of fatty liver disease. Pharmacol Ther 2017; 179: 142–57.
22. Arab JP, Karpen SJ, Dawson PA et al. Bile acids and nonalcoholic fatty liver disease: molecular insights and therapeutic perspectives. Hepatology 2017; 65: 350–62.
23. Amigo L, Husche C, Zanlungo S et al. Cholecystectomy increases hepatic triglyceride content and very-low-density lipoproteins production in mice. Liver Int 2011; 31: 52–64.
24. Portincasa P, Di Ciaula A, Wang HH et al. Coordinate regulation of gallbladder motor function in the gut-liver axis. Hepatology 2008; 47: 2112–26.
25. Roda E, Aldini R, Mazzella G et al. Enterohepatic circulation of bile acids after cholecystectomy. Gut 1978; 19: 640–9.
26. Deutschmann K, Reich M, Klindt C et al. Bile acid receptors in the biliary tree: TGR5 in physiology and disease. Biochim Biophys Acta 2017.
27. Inagaki T, Choi M, Moschetta A et al. Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis. Cell Metab 2005; 2: 217–25.
28. Kliewer SA, Mangelsdorf DJ. Bile acids as hormones: the FXR-FGF15/19 pathway. Dig Dis 2015; 33: 327–31.
29. Barrera F, Azocar L, Molina H et al. Effect of cholecystectomy on bile acid synthesis and circulating levels of fibroblast growth factor 19. Ann Hepatol 2015; 14: 710–21.
30. Wojcik M, Janus D, Dolezal-Oltarzewska K et al. A decrease in fasting FGF19 levels is associated with the development of nonalcoholic fatty liver disease in obese adolescents. J Pediat Endocrinol Metab 2012; 25 (11–12): 1089–93.
31. Pols TW, Noriega LG, Nomura M et al. The bile acid membrane receptor TGR5: a valuable metabolic target. Dig Dis 2011; 29: 37–44.
32. Keitel V, Haussinger D. Perspective: TGR5 (Gpbar-1) in liver physiology and disease. Clin Res Hepatol Gastroenterol 2012; 36: 412–19.
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[Lebedeva O.V., Bueverov A.O., Bueverova E.L., Nikitina L.O. Vliianie kholetsistektomii v molodom vozraste na techenie metabolicheskogo sindroma u zhenshchin. Al'manakh klin. med. 2017; 45 (6): 326–33 (in Russian).]
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32. Keitel V, Haussinger D. Perspective: TGR5 (Gpbar-1) in liver physiology and disease. Clin Res Hepatol Gastroenterol 2012; 36: 412–19.
33. Thomas C, Gioiello A, Noriega L et al. TGR5-mediated bile acid sensing controls glucose homeostasis. Cell Metab 2009; 10: 167–77.
34. Jones SA. Physiology of FGF15/19. Adv Exp Med Biol 2012; 728: 171–82.
35. Matsubara T, Li F, Gonzalez FJ. FXR signaling in the enterohepatic system. Mol Cell Endocrinol 2013; 368 (1–2): 17–29.
36. Cortes V, Quezada N, Uribe S et al. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in nonobese Hispanic patients: a pilot study. Lipids in health and disease 2017; 16: 129.
37. Lebedeva O.V., Bueverov A.O., Bueverova E.L., Nikitina L.O. Vliianie kholetsistektomii v molodom vozraste na techenie metabolicheskogo sindroma u zhenshchin. Al'manakh klin. med. 2017; 45 (6): 326–33 (in Russian).
38. Ruhl CE, Everhart JE. Relationship of nonalcoholic fatty liver disease with cholecystectomy in the US population. Am J Gastroenterol 2013; 108: 952–8.
39. Ioannou GN. Cholelithiasis, cholecystectomy, and liver disease. Am J Gastroenterol 2010; 105: 1364–73.
40. Kwak MS, Kim D, Chung GE et al. Cholecystectomy is independently associated with nonalcoholic fatty liver disease in an Asian population. World J Gastroenterol 2015; 21: 6287–95.
41. Yun S, Choi D, Lee KG et al. Cholecystectomy causes ultrasound evidence of increased hepatic steatosis. World J Surg 2016; 40: 1412–21.
42. Nervi F, Arrese M. Cholecystectomy and NAFLD: does gallbladder removal have metabolic consequences? Am J Gastroenterol 2013; 108: 959–61.
43. Shen C, Wu X, Xu C et al. Association of cholecystectomy with metabolic syndrome in a Chinese population. PloS One 2014; 9: e88189.
44. Hajong R, Dhal MR, Naku N et al. Incidence of nonalcoholic fatty liver disease in patients undergoing laparoscopic cholecystectomy. J Family Med Prim Care 2018; 7 (6): 1375–8.
45. Khaw KBC, Choi RH, Kam JH et al. Interval increase in the prevalence of symptomatic cholelithiasis-associated non-alcoholic fatty liver disease over a ten-year period in an Asian population. Singapore Med J 2017; 58 (12): 703–7.
46. Guo L, Mao J, Li Y et al. Cholelithiasis, cholecystectomy and risk of hepatocellular carcinoma: a meta-analysis. J Cancer Res Ther 2014; 10 (4): 834–8.
47. Chen Y, Wu S, Tian Y et al. Cholecystectomy as a risk factor of metabolic syndrome: from epidemiologic clues to biochemical mechanisms. Lab Invest 2018; 98 (1): 7–14.
48. Ratziu V, de Ledinghen V, Oberti F et al. A randomized controlled trial of high-dose ursodesoxycholic acid for nonalcoholic steatohepatitis. J Hepatol 2011; 54 (5): 1011–9.
49. Leuschner UF, Lindenthal B, Herrmann G et al. NASH Study Group. High-dose ursodeoxycholic acid therapy for nonalcoholic steatohepatitis: a double-blind, randomized, placebo-controlled trial. Hepatology 2010; 52 (2): 472–9.
50. Xiang Z, Chen YP, Ma KF et al. The role of ursodeoxycholic acid in non-alcoholic steatohepatitis: a systematic review. BMC Gastroenterol 2013; 13: 140.
51. Stokes CS, Gluud LL, Casper M, Lammert F. Ursodeoxycholic acid and diets higher in fat prevent gallbladder stones during weight loss: a meta-analysis of randomized controlled trials. Clin Gastroenterol Hepatol 2014; 12 (7): 1090–100.
Авторы
А.О. Буеверов
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия;
ГБУЗ МО «Московский областной научно-исследовательский клинический институт им. М.Ф. Владимирского», Москва, Россия;
АО «Группа компаний Объединенные медицинские системы», Москва, Россия
bcl72@yandex.ru
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия;
ГБУЗ МО «Московский областной научно-исследовательский клинический институт им. М.Ф. Владимирского», Москва, Россия;
АО «Группа компаний Объединенные медицинские системы», Москва, Россия
bcl72@yandex.ru
________________________________________________
Aleksei O. Bueverov
Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia;
Vladimirskiy Moscow Regional Research Clinical Institute, Moscow, Russia;
United Medical Systems Group of Companies, Moscow, Russia
bcl72@yandex.ru
Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia;
Vladimirskiy Moscow Regional Research Clinical Institute, Moscow, Russia;
United Medical Systems Group of Companies, Moscow, Russia
bcl72@yandex.ru
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