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Взаимосвязь сахарного диабета и неалкогольной жировой болезни печени: клинико-инструментальное парное исследование
Взаимосвязь сахарного диабета и неалкогольной жировой болезни печени: клинико-инструментальное парное исследование
Сасунова А.Н., Гончаров А.А., Гаппарова К.М., Исаков В.А. Взаимосвязь сахарного диабета и неалкогольной жировой болезни печени: клинико-инструментальное парное исследование. Терапевтический архив. 2024;96(8):764–770. DOI: 10.26442/00403660.2024.08.202810
© ООО «КОНСИЛИУМ МЕДИКУМ», 2024 г.
© ООО «КОНСИЛИУМ МЕДИКУМ», 2024 г.
________________________________________________
Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Цель. Изучить влияние сахарного диабета 2-го типа (СД 2) на тяжесть стеатоза и фиброза печени у больных неалкогольной жировой болезнью печени (НАЖБП).
Материалы и методы. Для проведения парного исследования «случай-контроль» из 2989 пациентов, проходивших обследование в ФГБУН «ФИЦ питания и биотехнологии», сформированы пары, совпадающие по полу и возрасту, распределенные по группам: НАЖБП + СД 2+ (n=313), НАЖБП + СД 2- (n=313) и контрольная группа пациентов без НАЖБП и без СД 2 (n=313). Выраженность стеатоза печени определялась при помощи измерения контролируемого параметра затухания ультразвуковой волны, выраженность фиброза печени оценивалась при помощи определения показателя эластичности печени. Состав тела пациентов изучался с использованием биоимпедансометрии. Показатели липидного и углеводного обмена, а также активность ферментов печени в сыворотке крови определялись стандартными биохимическими методами.
Результаты. При сравнении антропометрических показателей в группе НАЖБП + СД 2+ по сравнению с группой НАЖБП + СД 2-, а у последней – по сравнению с контрольной группой оказались выше масса тела, индекс массы тела, окружность талии и бедер, соотношение талии к бедрам. При этом в группах НАЖБП + СД 2+ и НАЖБП + СД 2- объем жировой массы прямо коррелировал с уровнем триглицеридов крови (r=0,21), гликированного гемоглобина (r=0,32), глюкозы крови натощак (r=0,35) и обратно – с липопротеидами высокой плотности (r=-0,19). При оценке выраженности стеатоза и фиброза печени в группе НАЖБП + СД 2+ по сравнению с группой НАЖБП + СД 2- тяжелая степень стеатоза (S3, 78% против 59,4%; p<0,001) и тяжелая степень фиброза печени (F4, 8% против 2,6%; p<0,001) встречались чаще. При этом у 70% пациентов группы НАЖБП + СД 2- по данным эластографии фиброз печени отсутствовал (F0), в то же время в группе НАЖБП + СД 2+ в эту категорию попадали только 43,2% пациентов (p<0,0001).
Заключение. При присоединении к НАЖБП СД 2 наблюдается увеличение общей жировой массы, выраженности стеатоза и фиброза печени и связанного с ними ухудшения показателей липидного обмена. Более чем у 1/2 таких пациентов имеется фиброз печени различных стадий, что указывает на прогрессирующий характер заболевания.
Ключевые слова: неалкогольная жировая болезнь печени, сахарный диабет 2-го типа, фиброз печени, стеатоз печени
Materials and methods. To conduct a paired case-control study 2989 patients were examined at the Federal Research Center of Nutrition, Biotechnology and Food Safety. Pairs were matched by gender and age and distributed into groups: NAFLD + DM2+ (n=313), NAFLD + DM2- (n=313) and a control group of patients without NAFLD and without DM2 (n=313). The severity of liver steatosis was determined by measuring the controlled attenuation parameter. The severity of liver fibrosis was determined by measuring the liver stiffness measurement. Body composition of the patients was determined using bioimpedance measurements. Indicators of lipid and carbohydrate metabolism, and the serum activity of liver enzymes was determined by standard biochemical methods.
Results. In NAFLD + DM2+ group compared to NAFLD + DM2- group, and in NAFLDM + DM2-compared to the control group, weight, BMI, waist and hip circumference, waist-to-hip ratio were higher, while in all. In NAFLD + DM2+ and NAFLD + DM2- groups the volume of fat mass directly correlated with the level of blood triglycerides (r=0.21), HbA1с (r=0.32) and fasting blood glucose (r=0.35), and inversely correlated with high-density lipoproteins (r=-0.19). In NAFLD + DM2+ group versus NAFLD + DM2- group severe steatosis (S3, 78% versus 59.4%; p<0.001) and severe fibrosis (F4, 8% vs 2.6%; p<0.001) was more common; 70% of patients in the NAFLD + DM2- group had no liver fibrosis according to elastography (F0), while in the NAFLD + DM2+ group only 43.2% of patients had no liver fibrosis (p<0.0001).
Conclusion. When NAFLD is accompanied by DM2, there is an increase in total fat mass, the severity of steatosis and liver fibrosis, and an associated deterioration of lipid metabolism. More than half of these patients have various stages of liver fibrosis, which indicates the progressive nature of the disease.
Keywords: non-alcoholic fatty liver disease, type 2 diabetes mellitus, liver fibrosis, hepatic steatosis
Материалы и методы. Для проведения парного исследования «случай-контроль» из 2989 пациентов, проходивших обследование в ФГБУН «ФИЦ питания и биотехнологии», сформированы пары, совпадающие по полу и возрасту, распределенные по группам: НАЖБП + СД 2+ (n=313), НАЖБП + СД 2- (n=313) и контрольная группа пациентов без НАЖБП и без СД 2 (n=313). Выраженность стеатоза печени определялась при помощи измерения контролируемого параметра затухания ультразвуковой волны, выраженность фиброза печени оценивалась при помощи определения показателя эластичности печени. Состав тела пациентов изучался с использованием биоимпедансометрии. Показатели липидного и углеводного обмена, а также активность ферментов печени в сыворотке крови определялись стандартными биохимическими методами.
Результаты. При сравнении антропометрических показателей в группе НАЖБП + СД 2+ по сравнению с группой НАЖБП + СД 2-, а у последней – по сравнению с контрольной группой оказались выше масса тела, индекс массы тела, окружность талии и бедер, соотношение талии к бедрам. При этом в группах НАЖБП + СД 2+ и НАЖБП + СД 2- объем жировой массы прямо коррелировал с уровнем триглицеридов крови (r=0,21), гликированного гемоглобина (r=0,32), глюкозы крови натощак (r=0,35) и обратно – с липопротеидами высокой плотности (r=-0,19). При оценке выраженности стеатоза и фиброза печени в группе НАЖБП + СД 2+ по сравнению с группой НАЖБП + СД 2- тяжелая степень стеатоза (S3, 78% против 59,4%; p<0,001) и тяжелая степень фиброза печени (F4, 8% против 2,6%; p<0,001) встречались чаще. При этом у 70% пациентов группы НАЖБП + СД 2- по данным эластографии фиброз печени отсутствовал (F0), в то же время в группе НАЖБП + СД 2+ в эту категорию попадали только 43,2% пациентов (p<0,0001).
Заключение. При присоединении к НАЖБП СД 2 наблюдается увеличение общей жировой массы, выраженности стеатоза и фиброза печени и связанного с ними ухудшения показателей липидного обмена. Более чем у 1/2 таких пациентов имеется фиброз печени различных стадий, что указывает на прогрессирующий характер заболевания.
Ключевые слова: неалкогольная жировая болезнь печени, сахарный диабет 2-го типа, фиброз печени, стеатоз печени
________________________________________________
Materials and methods. To conduct a paired case-control study 2989 patients were examined at the Federal Research Center of Nutrition, Biotechnology and Food Safety. Pairs were matched by gender and age and distributed into groups: NAFLD + DM2+ (n=313), NAFLD + DM2- (n=313) and a control group of patients without NAFLD and without DM2 (n=313). The severity of liver steatosis was determined by measuring the controlled attenuation parameter. The severity of liver fibrosis was determined by measuring the liver stiffness measurement. Body composition of the patients was determined using bioimpedance measurements. Indicators of lipid and carbohydrate metabolism, and the serum activity of liver enzymes was determined by standard biochemical methods.
Results. In NAFLD + DM2+ group compared to NAFLD + DM2- group, and in NAFLDM + DM2-compared to the control group, weight, BMI, waist and hip circumference, waist-to-hip ratio were higher, while in all. In NAFLD + DM2+ and NAFLD + DM2- groups the volume of fat mass directly correlated with the level of blood triglycerides (r=0.21), HbA1с (r=0.32) and fasting blood glucose (r=0.35), and inversely correlated with high-density lipoproteins (r=-0.19). In NAFLD + DM2+ group versus NAFLD + DM2- group severe steatosis (S3, 78% versus 59.4%; p<0.001) and severe fibrosis (F4, 8% vs 2.6%; p<0.001) was more common; 70% of patients in the NAFLD + DM2- group had no liver fibrosis according to elastography (F0), while in the NAFLD + DM2+ group only 43.2% of patients had no liver fibrosis (p<0.0001).
Conclusion. When NAFLD is accompanied by DM2, there is an increase in total fat mass, the severity of steatosis and liver fibrosis, and an associated deterioration of lipid metabolism. More than half of these patients have various stages of liver fibrosis, which indicates the progressive nature of the disease.
Keywords: non-alcoholic fatty liver disease, type 2 diabetes mellitus, liver fibrosis, hepatic steatosis
Полный текст
Список литературы
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10. Ryysy L, Häkkinen AM, Goto T, et al. Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patients. Diabetes. 2000;49(5):749-58. DOI:10.2337/diabetes.49.5.749
11. Kotronen A, Juurinen L, Tiikkainen M, et al. Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. Gastroenterology. 2008;135(1):122-30. DOI:10.1053/j.gastro.2008.03.021
12. Gastaldelli A, Cusi K. From NASH to diabetes and from diabetes to NASH: Mechanisms and treatment options. JHEP Rep. 2019;1(4):312-28. DOI:10.1016/j.jhepr.2019.07.002
13. 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. Diabetologia. 2016;59(6):1121-40. DOI:10.1007/s00125-016-3902-y
14. Shih CI, Wu KT, Hsieh MH, et al. Severity of fatty liver is highly correlated with the risk of hypertension and diabetes: a cross-sectional and longitudinal cohort study. Hepatol Int. 2024;18(1):138-54. DOI:10.1007/s12072-023-10576-z
15. Sinn DH, Kang D, Guallar E, et al. Regression of nonalcoholic fatty liver disease is associated with reduced risk of incident diabetes: A longitudinal cohort study. PLoS One. 2023;18(7):e0288820. DOI:10.1371/journal.pone.0288820
16. Dulai PS, Singh S, Patel J, et al. Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and metaanalysis. Hepatology. 2017;65(5):1557-65. DOI:10.1002/hep.29085
17. Ng CH, Lim WH, Hui Lim GE, et al. Mortality Outcomes by Fibrosis Stage in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2023;21(4):931-9.e5. DOI:10.1016/j.cgh.2022.04.014
18. Newsome PN, Buchholtz K, Cusi K, et al. A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. N Engl J Med. 2021;384(12):1113-24. DOI:10.1056/NEJMoa2028395
19. Ghosal S, Datta D, Sinha B. A meta-analysis of the effects of glucagon-like-peptide 1 receptor agonist (GLP1-RA) in nonalcoholic fatty liver disease (NAFLD) with type 2 diabetes (T2D). Sci Rep. 2021;11(1):22063. DOI:10.1038/s41598-021-01663-y
2. Williamson RM, Price JF, Glancy S, et al. Prevalence of and risk factors for hepatic steatosis and non-alcoholic fatty liver disease in people with type 2 diabetes: the Edinburgh Type 2 Diabetes Study. Diabetes Care. 2011;34(5):1139-44. DOI:10.2337/dc10-2229
3. Kotronen A, Juurinen L, Hakkarainen A, et al. Liver fat is increased in type 2 diabetic patients and underestimated by serum alanine amino-transferase compared with equally obese non diabetic subjects. Diabetes Care. 2008;31(1):165-9. DOI:10.2337/dc07-1463
4. Targher G, Byrne CD. Clinical Review: Non-alcoholic fatty liver disease: a novel cardiometabolic risk factor for type 2 diabetes and its complications. J Clin Endocrinol Metab. 2013;98(2):483-95. DOI:10.1210/jc.2012-3093
5. Dharmalingam M, Yamasandhi PG. Non-alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus. Indian J Endocrinol Metab. 2018;22(3):421-8. DOI:10.4103/ijem.IJEM_585_17
6. Sanyal AJ, Chalasani N, Kowdley KV, et al. Pioglitazone, vitamin E, or placebo for non-alcoholic steatohepatitis. N Engl J Med. 2010;362(18):1675-85. DOI:10.1056/NEJMoa0907929
7. Karlas T, Petroff D, Sasso M, et al. Individual patient data meta-analysis of controlled attenuation parameter (CAP) technology for assessing steatosis. J Hepatol. 2017;66(5):1022-30. DOI:10.1016/j.jhep.2016.12.022
8. Tsochatzis EA, Gurusamy KS, Ntaoula S. et al. Elastography for the diagnosis of severity of fibrosis in chronic liver disease: a meta-analysis of diagnostic accuracy. J Hepatol. 2011;54(4):650-9. DOI:10.1016/j.jhep.2010.07.033
9. Parry SA, Hodson L. Managing NAFLD in Type 2 Diabetes: The Effect of Lifestyle Interventions, a Narrative Review. Adv Ther. 2020;37(4):1381-406. DOI:10.1007/s12325-020-01281-6
10. Ryysy L, Häkkinen AM, Goto T, et al. Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patients. Diabetes. 2000;49(5):749-58. DOI:10.2337/diabetes.49.5.749
11. Kotronen A, Juurinen L, Tiikkainen M, et al. Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. Gastroenterology. 2008;135(1):122-30. DOI:10.1053/j.gastro.2008.03.021
12. Gastaldelli A, Cusi K. From NASH to diabetes and from diabetes to NASH: Mechanisms and treatment options. JHEP Rep. 2019;1(4):312-28. DOI:10.1016/j.jhepr.2019.07.002
13. 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. Diabetologia. 2016;59(6):1121-40. DOI:10.1007/s00125-016-3902-y
14. Shih CI, Wu KT, Hsieh MH, et al. Severity of fatty liver is highly correlated with the risk of hypertension and diabetes: a cross-sectional and longitudinal cohort study. Hepatol Int. 2024;18(1):138-54. DOI:10.1007/s12072-023-10576-z
15. Sinn DH, Kang D, Guallar E, et al. Regression of nonalcoholic fatty liver disease is associated with reduced risk of incident diabetes: A longitudinal cohort study. PLoS One. 2023;18(7):e0288820. DOI:10.1371/journal.pone.0288820
16. Dulai PS, Singh S, Patel J, et al. Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and metaanalysis. Hepatology. 2017;65(5):1557-65. DOI:10.1002/hep.29085
17. Ng CH, Lim WH, Hui Lim GE, et al. Mortality Outcomes by Fibrosis Stage in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2023;21(4):931-9.e5. DOI:10.1016/j.cgh.2022.04.014
18. Newsome PN, Buchholtz K, Cusi K, et al. A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. N Engl J Med. 2021;384(12):1113-24. DOI:10.1056/NEJMoa2028395
19. Ghosal S, Datta D, Sinha B. A meta-analysis of the effects of glucagon-like-peptide 1 receptor agonist (GLP1-RA) in nonalcoholic fatty liver disease (NAFLD) with type 2 diabetes (T2D). Sci Rep. 2021;11(1):22063. DOI:10.1038/s41598-021-01663-y
2. Williamson RM, Price JF, Glancy S, et al. Prevalence of and risk factors for hepatic steatosis and non-alcoholic fatty liver disease in people with type 2 diabetes: the Edinburgh Type 2 Diabetes Study. Diabetes Care. 2011;34(5):1139-44. DOI:10.2337/dc10-2229
3. Kotronen A, Juurinen L, Hakkarainen A, et al. Liver fat is increased in type 2 diabetic patients and underestimated by serum alanine amino-transferase compared with equally obese non diabetic subjects. Diabetes Care. 2008;31(1):165-9. DOI:10.2337/dc07-1463
4. Targher G, Byrne CD. Clinical Review: Non-alcoholic fatty liver disease: a novel cardiometabolic risk factor for type 2 diabetes and its complications. J Clin Endocrinol Metab. 2013;98(2):483-95. DOI:10.1210/jc.2012-3093
5. Dharmalingam M, Yamasandhi PG. Non-alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus. Indian J Endocrinol Metab. 2018;22(3):421-8. DOI:10.4103/ijem.IJEM_585_17
6. Sanyal AJ, Chalasani N, Kowdley KV, et al. Pioglitazone, vitamin E, or placebo for non-alcoholic steatohepatitis. N Engl J Med. 2010;362(18):1675-85. DOI:10.1056/NEJMoa0907929
7. Karlas T, Petroff D, Sasso M, et al. Individual patient data meta-analysis of controlled attenuation parameter (CAP) technology for assessing steatosis. J Hepatol. 2017;66(5):1022-30. DOI:10.1016/j.jhep.2016.12.022
8. Tsochatzis EA, Gurusamy KS, Ntaoula S. et al. Elastography for the diagnosis of severity of fibrosis in chronic liver disease: a meta-analysis of diagnostic accuracy. J Hepatol. 2011;54(4):650-9. DOI:10.1016/j.jhep.2010.07.033
9. Parry SA, Hodson L. Managing NAFLD in Type 2 Diabetes: The Effect of Lifestyle Interventions, a Narrative Review. Adv Ther. 2020;37(4):1381-406. DOI:10.1007/s12325-020-01281-6
10. Ryysy L, Häkkinen AM, Goto T, et al. Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patients. Diabetes. 2000;49(5):749-58. DOI:10.2337/diabetes.49.5.749
11. Kotronen A, Juurinen L, Tiikkainen M, et al. Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. Gastroenterology. 2008;135(1):122-30. DOI:10.1053/j.gastro.2008.03.021
12. Gastaldelli A, Cusi K. From NASH to diabetes and from diabetes to NASH: Mechanisms and treatment options. JHEP Rep. 2019;1(4):312-28. DOI:10.1016/j.jhepr.2019.07.002
13. 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. Diabetologia. 2016;59(6):1121-40. DOI:10.1007/s00125-016-3902-y
14. Shih CI, Wu KT, Hsieh MH, et al. Severity of fatty liver is highly correlated with the risk of hypertension and diabetes: a cross-sectional and longitudinal cohort study. Hepatol Int. 2024;18(1):138-54. DOI:10.1007/s12072-023-10576-z
15. Sinn DH, Kang D, Guallar E, et al. Regression of nonalcoholic fatty liver disease is associated with reduced risk of incident diabetes: A longitudinal cohort study. PLoS One. 2023;18(7):e0288820. DOI:10.1371/journal.pone.0288820
16. Dulai PS, Singh S, Patel J, et al. Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and metaanalysis. Hepatology. 2017;65(5):1557-65. DOI:10.1002/hep.29085
17. Ng CH, Lim WH, Hui Lim GE, et al. Mortality Outcomes by Fibrosis Stage in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2023;21(4):931-9.e5. DOI:10.1016/j.cgh.2022.04.014
18. Newsome PN, Buchholtz K, Cusi K, et al. A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. N Engl J Med. 2021;384(12):1113-24. DOI:10.1056/NEJMoa2028395
19. Ghosal S, Datta D, Sinha B. A meta-analysis of the effects of glucagon-like-peptide 1 receptor agonist (GLP1-RA) in nonalcoholic fatty liver disease (NAFLD) with type 2 diabetes (T2D). Sci Rep. 2021;11(1):22063. DOI:10.1038/s41598-021-01663-y
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2. Williamson RM, Price JF, Glancy S, et al. Prevalence of and risk factors for hepatic steatosis and non-alcoholic fatty liver disease in people with type 2 diabetes: the Edinburgh Type 2 Diabetes Study. Diabetes Care. 2011;34(5):1139-44. DOI:10.2337/dc10-2229
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Авторы
А.Н. Сасунова, А.А. Гончаров*, К.М. Гаппарова, В.А. Исаков
ФГБУН «Федеральный исследовательский центр питания, биотехнологии и безопасности пищи», Москва, Россия
*thisalexis@gmail.com
Federal Research Center of Nutrition, Biotechnology and Food Safety, Moscow, Russia
*thisalexis@gmail.com
ФГБУН «Федеральный исследовательский центр питания, биотехнологии и безопасности пищи», Москва, Россия
*thisalexis@gmail.com
________________________________________________
Federal Research Center of Nutrition, Biotechnology and Food Safety, Moscow, Russia
*thisalexis@gmail.com
Цель портала OmniDoctor – предоставление профессиональной информации врачам, провизорам и фармацевтам.