scholarly journals THE POSITRON EMISSION TOMOGRAPHY IN EARLY DIAGNOSTICS OF THE METABOLIC MYOCARDIAL DISORDERS IN INSULIN-RESISTANT PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE

2020 ◽  
Vol 17 (34) ◽  
pp. 1026-1032
Author(s):  
Grigory Efimovich ROYTBERG ◽  
Olga Olegovna SHARKHUN ◽  
Oksana Evgenyevna PLATONOVA ◽  
Anna Alexandrovna STEPANOVA
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Cardiac Remodeling ◽  
Fatty Liver Disease ◽  
Emission Tomography ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Positron Emission ◽  
Alcoholic Fatty Liver Disease

Recent studies demonstrated the Hepato-cardiac relationship in patients with non-alcoholic fatty liver disease as subclinical, structural, and functional alterations in the heart. However, the mechanisms underlying the changes in the cardiovascular system are understudied and not clear. The aim of the study was to assess glucose metabolism, its perfusion in the cardiomyocytes and the detection of the myocardial dysfunction in patients with fatty liver disease and insulin resistance using the positron emission tomography with fludeoxyglucose. During the study, 18 patients (14 men and 4 women, mean age 52 ± 4.2 years) with the non-alcoholic fatty liver disease and the insulin resistance (HOMA-IR>2.6) were examined. There were 12 patients in the control group. Echocardiography revealed various types of the left ventricular cardiac remodeling in the study group: 44.4% of patients with eccentric hypertrophy, 38.9% with concentric hypertrophy, and 16.7% with the concentric remodeling. In this group, there was a pronounced diffuse uneven distribution of the radiopharmaceutical. In addition, zones of hypometabolism and paradoxical accumulation of glucose were detected. Thus, it was shown that in patients with non-alcoholic fatty liver disease and insulin resistance, the intensity and nature of glucose metabolism in cardiomyocytes changed, indicating the presence of myocardial metabolic dysfunction. We believe that the systemic insulin resistance metabolic processes were disturbed not only in the liver cells but also in the cardiomyocytes. As a result of the metabolic dysfunction, the geometric parameters of the heart are changed, and various types of cardiac remodeling are formed.

scholarly journals Non-alcoholic fatty liver disease and the myocardial remodeling: the role of insulin resistance in the hepatocardial association development

2020 ◽  
Vol 174 (5) ◽  
pp. 47-52
Author(s):  
G. E. Rojtberg ◽  
O. O. Sharkhun
Keyword(s):  
Insulin Resistance ◽  
Positron Emission Tomography ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Myocardial Dysfunction ◽  
Emission Tomography ◽  
Alcoholic Fatty Liver ◽  
Positron Emission ◽  
Alcoholic Fatty Liver Disease

Aim. The aim of the study was to assess glucose metabolism, its perfusion in the cardiomyocytes and the detection of the myocardial dysfunction in patients with fatty liver disease and insulin resistance using the positron emission tomography with fl udeoxyglucose. Materials and methods. In our study patients with the non-alcoholic fatty liver disease and the insulin resistance were examined. All patients underwent the еchocardiography and the positron emission tomography scans for myocardial dysfunction assessment. Results and discussion. Echocardiography revealed various types of the left ventricular cardiac remodeling. The positron emission tomography showed a pronounced diffuse uneven distribution of the radiopharmaceutical. In addition, zones of hypometabolism and paradoxical accumulation of glucose were detected. It`s important to note that these indicated zones did not form sectors around a specifi c artery area, possibly refl ecting zones of fatty infi ltration or fi brotic changes in the myocardium. Thus, it was shown that in patients with the non-alcoholic fatty liver disease and insulin resistance the intensity and nature of glucose metabolism in cardiomyocytes were changed, indicating the presence of myocardial metabolic dysfunction. Conclusion. We believe that in systemic insulin resistance metabolic processes were disturbed not only in the liver cells, but also in the cardiomyocytes, the rate of glucose utilization and its transmembrane transfer into cardiomyocytes were changed. As a result of the metabolic dysfunction, the geometric parameters of the heart are changed and various types of the cardiac remodelling are formed.

Non-Alcoholic Fatty Liver Disease in Overweight Children and its Relationship with Retinol Serum Levels

2008 ◽  
Vol 78 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Suano de Souza ◽  
Silverio Amancio ◽  
Saccardo Sarni ◽  
Sacchi Pitta ◽  
Fernandes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Profile ◽  
Fatty Liver Disease ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Objectives: To evaluate the frequency of non-alcoholic fatty liver disease, the retinol serum levels, lipid profile, and insulin resistance in overweight/obese children. To relate these biochemical variables with the risk of this disease in the population studied. Methods: The study was cross-sectional and prospective, with 46 overweight/obese school children (28 female, 18 male; mean age 8.6 years). The control group consisted of 45 children, paired by age and gender. Hepatic steatosis, evaluated by ultrasound, was classified as normal, mild, moderate, or severe. Also evaluated were serum retinol levels; thiobarbituric acid reactive substances; lipid profile; and fasting glucose and serum insulin levels, used for the calculation of the Homeostasis Model Assessment. Results: Hepatic ultrasound alterations were found in 56.5% and 48,9% of the overweight/obese and control group children, respectively. Presence of obesity was associated with high levels of triglycerides (OR = 4.6; P = 0.002). In the studied children, the risk of steatosis was related to a trend to a higher percentage of retinol inadequacy (OR = 2.8; p = 0.051); there was no association with thiobarbituric acid reactive substances, lipid profile, or insulin resistance. Conclusions: The high frequency of non-alcoholic fatty liver disease in both groups, evaluated by hepatic ultrasound, in low-socioeconomic level children, independent of nutritional condition and without significant association with insulin resistance, emphasizes that especially in developing countries, other risk factors such as micronutrient deficiencies (e.g. vitamin A) are involved.

Non-alcoholic fatty liver disease and its association with insulin resistance in an obese population

2018 ◽  
Author(s):  
Frederique Van de Velde ◽  
Marlies Bekaert ◽  
Anne Hoorens ◽  
Marleen Praet ◽  
Arsene-Helene Batens ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Obese Population ◽  
Alcoholic Fatty Liver Disease

scholarly journals Role of Insulin Resistance in MAFLD

2021 ◽  
Vol 22 (8) ◽  
pp. 4156
Author(s):  
Yoshitaka Sakurai ◽  
Naoto Kubota ◽  
Toshimasa Yamauchi ◽  
Takashi Kadowaki
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo Lipogenesis ◽  
Hepatic Insulin Resistance ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD.

scholarly journals Higher Sodium Intake Assessed by 24 Hour Urinary Sodium Excretion Is Associated with Non-Alcoholic Fatty Liver Disease: The PREVEND Cohort Study

2019 ◽  
Vol 8 (12) ◽  
pp. 2157 ◽  
Author(s):  
Eline H. van den Berg ◽  
Eke G. Gruppen ◽  
Hans Blokzijl ◽  
Stephan J.L. Bakker ◽  
Robin P.F. Dullaart
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Sodium Excretion ◽  
Fatty Liver Disease ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Model Assessment ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Dietary sodium intake was measured by sodium excretion in two complete consecutive 24 h urine collections in 6132 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Fatty Liver Index (FLI) ≥60 and Hepatic Steatosis Index (HSI) >36 were used as proxies of suspected NAFLD. 1936 (31.6%) participants had an FLI ≥60, coinciding with the increased prevalence of type 2 diabetes (T2D), metabolic syndrome, hypertension and history of cardiovascular disease. Sodium intake was higher in participants with an FLI ≥60 (163.63 ± 61.81 mmol/24 h vs. 136.76 ± 50.90 mmol/24 h, p < 0.001), with increasing incidence in ascending quartile categories of sodium intake (p < 0.001). Multivariably, an FLI ≥60 was positively associated with a higher sodium intake when taking account for T2D, a positive cardiovascular history, hypertension, alcohol intake, smoking and medication use (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.44–1.64, p < 0.001). Additional adjustment for the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) diminished this association (OR 1.30, 95% CI 1.21–1.41, p < 0.001). HSI >36 showed similar results. Associations remained essentially unaltered after adjustment for body surface area or waist/hip ratio. In conclusion, suspected NAFLD is a feature of higher sodium intake. Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake.

scholarly journals Beneficial effect of omarigliptin on diabetic patients with non-alcoholic fatty liver disease/non-alcoholic steatohepatitis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Sachiko Hattori ◽  
Kazuomi Nomoto ◽  
Tomohiko Suzuki ◽  
Seishu Hayashi
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Liver Function ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Hepatic Insulin Resistance ◽  
Diabetic Patients ◽  
Alcoholic Fatty Liver ◽  
Dpp4 Inhibitor ◽  
Alcoholic Fatty Liver Disease

Abstract Background Dipeptidyl peptidase 4 (DPP4) is a serine exopeptidase able to inactivate various oligopeptides, and also a hepatokine. Hepatocyte-specific overexpression of DPP4 is associated with hepatic insulin resistance and liver steatosis. Method We examined whether weekly DPP4 inhibitor omarigliptin (OMG) can improve liver function as well as levels of inflammation and insulin resistance in type 2 diabetic patients with non-alcoholic fatty liver disease (NAFLD). Further, we investigated the effects of OMG in a diabetic patient with biopsy-confirmed nonalcoholic steatohepatitis (NASH). Results In NAFLD patients, OMG significantly decreased levels of aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, homeostatic model assessment of insulin resistance (HOMA-IR), and high-sensitivity C-reactive protein (hsCRP), while no significant change was seen in hemoglobin A1c or body mass index. In the NASH patient, liver function improved markedly, and levels of the hepatic fibrosis marker FIB-4 decreased in parallel with HOMA-IR and hsCRP. Slight but clear improvements in intrahepatic fat deposition and fibrosis appeared to be seen on diagnostic ultrasonography. Conclusion Weekly administration of the DPP4 inhibitor OMG in ameliorating hepatic insulin resistance may cause beneficial effects in liver with NAFLD/NASH.

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