De Novo Lipogenesis in Severity of NAFLD
Nonalcoholic Fatty Liver DiseaseNonalcoholic Steatohepatitis3 moreNAFLD is the most prevalent liver disease in the U.S., and there is a serious need to understand its progression to the advanced state, nonalcoholic steatohepatitis (NASH). Previous studies has shown that elevated de novo lipogenesis (DNL) is the unique, early event distinguishing patients with NAFLD from equally-obese subjects with low IHTG. The purpose of this study is to directly by measure DNL in human liver tissue and comparing it to liver histological scores from patient biopsies.
Biomarkers of Liver Pathology in Patients With Presumed Non-Alcoholic Steatohepatitis Following...
NASH - Nonalcoholic Steatohepatitis; NAFLD - Nonalcoholic Fatty Liver DiseaseThe purpose of this study is to evaluate imaging and other biomarkers of non-alcoholic fatty liver disease before and after bariatric surgery.
Serum Selenium and Zinc Levels in Non-alcoholic Fatty Liver Disease Patients
NAFLDNon-alcoholic fatty liver disease (NAFLD) includes a wide range of disorders that consist of simple fatty infiltration, steatohepatitis (NASH), and end-stage liver disease (cirrhosis). NAFLD is the most common cause of chronic liver disease worldwide and increases the risk of end-stage liver disease and hepatocellular carcinoma (HCC) . While risk factors such as obesity, diabetes, and a sedentary lifestyle may increase the risk of NAFLD, studies have shown that environmental exposures may further contribute to the pathogenesis of NAFLD. Although the pathogenic role of macronutrients is well established in both NAFLD and obesity, the contribution of micronutrients to NAFLD pathogenesis has garnered less attention than with obesity. Selenium is an essential element in many biological functions and is an important component of human nutrition. Exposure to selenium can be found in nature, such as rocks and sediment, air, soil, fuel oil, drinking water and nutritional supplementation. It is a major component of many enzymes such as glutathione peroxidase and plays an important role in anti-oxidation, DNA synthesis, reproduction, muscle function, and thyroid metabolism. Selenium concentrations have been studied in many diseases and organ systems including the liver. However, the exact relationship between selenium in patients with NAFLD is unclear. Selenium is an essential element in many biological functions and is an important component of human nutrition. It is a major component of many enzymes such as glutathione peroxidase and plays an important role in anti-oxidation, DNA synthesis, reproduction, muscle function, and thyroid metabolism. Selenium concentrations have been studied in many diseases and organ systems including the liver. However, the exact relationship between selenium in patients with NAFLD is unclear. Despite data suggesting mineral deficiencies in NAFLD patients, most data do not support insufficient mineral consumption as a possible mechanism for these deficiencies, except in the case of zinc deficiency. Zinc is the second most prevalent trace element in the body. It is integrally involved in the normal life cycle and has many important regulatory, catalytic, and defensive functions. Zinc deficiency occurs in many types of liver disease, especially more advanced/decompensated disease.
The Effect of Lifestyle-induced Hepatic Steatosis on Glucagon-stimulated Amino Acid Turnover
Non-Alcoholic Fatty Liver DiseaseGlucagon ResistanceMany patients with type 2 diabetes exhibit elevated plasma concentrations of the glucose-mobilising pancreatic hormone glucagon; i.e. hyperglucagonaemia. This contributes to the hyperglycaemic state of the patients and is considered an important component in the pathophysiology of type 2 diabetes; but the mechanisms underlying this phenomenon remain unclear. The liver constitutes the main target organ of glucagon, and studies have shown that hyperglucagonaemia goes hand in hand with hyperaminoacidaemia and that both are associated with non-alcoholic fatty liver disease (NAFLD), independently of the presence of type 2 diabetes. In line with this, several recent studies support the existence of a feedback-cycle between the liver and the pancreatic alpha cells, governed by circulating glucagon and amino acids. The investigators hypothesise that the presence of hepatic steatosis results in hepatic glucagon resistance at the level of amino acid turnover, i.e. impaired glucagon-induced suppression of circulating amino acid concentrations. If this hypothesis proves correct, it would establish build-up of fat in the liver as a core mechanism underlying hyperglucagonaemia and, since the hyperglucagonemia is at least partly responsible for the fasting hyperglycaemia, as an important contributor to the hyperglycaemia of type 2 diabetes.
Weight Gain After Smoking Cessation and NAFLD
Nonalcoholic Fatty Liver DiseaseType 2 DiabetesNonalcoholic fatty liver disease (NAFLD) is rapidly becoming the most common chronic liver disease. Considering that there are no approved pharmacological treatments, lifestyle modification is necessary and challenging to reduce the risk of type 2 diabetes mellitus (T2DM) in patients with NAFLD. Cigarette smoking has a significant negative impact on public health, causing more than 480,000 deaths each year. Smoking has been reported as a risk factor for NAFLD and might accelerate liver disease progression. Therefore, it is recommended that patients with NAFLD quit smoking. However, smoking cessation could be complicated by weight gain. Thus, it is important to assess the impact of weight change after smoking cessation on patients with NAFLD. Proper management of post-cessation weight could maximize its health benefits. In this large-scale cohort study, the investigators aimed to assess the effects of smoking cessation and subsequent weight change on risks of incident T2DM in individuals with NAFLD.
Web-based Interventions on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Children
NAFLDWeb1 moreThe web-based continuity of care intervention model to provide comprehensive nursing interventions for obese children with NAFLD, always tracking their performance status, enabling them to grasp the knowledge of healthy weight loss, develop good lifestyle habits, and reduce their weight, thus reducing the incidence of NAFLD in children.
The Liver Health Study for Patients With NAFLD
Nonalcoholic Fatty LiverNonalcoholic Steatohepatitis1 moreThe study will investigate whether the level of fat stored in the liver is related to the liver's ability to burn fat.
EUS Guided Core Liver Biopsy and IGB Placement for the Diagnosis and Management of NASH and Obesity...
ObesityNon-Alcoholic SteatohepatitisThis study is designed to investigate the impact of weight loss achieved with the IGB on NASH with early fibrosis in a select cohort of patients with obesity preselected to have a high pre-test probability of having NASH with early fibrosis based on magnetic resonance elastography (MRE)-Hepatogram. In addition, this study will explore potential non-invasive imaging criteria for NASH and early fibrosis using EUS-Elastography.
Glucose-induced Glucagon-like Peptide 1 (GLP-1) Secretion in NAFLD Patients Compared to Healthy...
Non Alcoholic Fatty Liver DiseaseNon Alcoholic SteatohepatitisThe incretin effect is impaired in patients with type 2 diabetes mellitus (T2DM), thus GLP-1 receptor agonists are used for the treatment of T2DM. Insulin resistance is a pathophysiologic hallmark of non-alcoholic fatty liver disease (NAFLD). The incretin effect in patients with NAFLD has not been studied. The aim of this study is to quantify GLP-1 secretion in response to oral glucose tolerance test (oGTT) in patients with NAFLD compared to healthy controls. The results of this study will expand the knowledge of the pathophysiology of NAFLD and serve as a rational for potential future treatment strategies.
Effect of Fructose Reduction on Non-alcoholic Fatty Liver Disease (NAFLD) and Metabolic Syndrome...
Non-alcoholic Fatty Liver DiseaseThe aim of the present study is to find out if a dietary intervention mainly focusing on fructose reduction has a preventive effect on the development and progression of NAFLD and the metabolic syndrome in overweight children.