View clinical trials related to Fatty Liver.
Filter by:The primary objective of this study is to evaluate the single-dose pharmacokinetics of cilofexor in adults with impaired hepatic function relative to matched, healthy controls with normal hepatic function.
The primary aim is to determine the accuracy of CAP in the quantification of liver steatosis using liver biopsies as reference. Secondarily, investigators will correlate transient elastography (TE) and CAP results, analyze possible associations between CAP/TE and post-liver transplant (LT) clinical outcomes, and evaluate the change in CAP after LT. The study aims to include as many donors as needed to achieve at least 120 transplanted liver allografts.
The purpose of this study is to determine the effects of a low carbohydrate diet vs a low fat diet on improvement in aminotransferases, hepatic fat infiltration, markers of inflammation, insulin resistance, and body composition in obese adolescents with non-alcoholic fatty liver disease (NAFLD).
Ultrasound (US) B mode image is an alternative method to measure tissue structure and has proven to be an accurate technique to measure subcutaneous fat thickness. However, pressing the transducer onto the skin with too much force will significantly reduce the subcutaneous adipose tissue thickness. In this study, a force controlled system combined with US transducer was used for 3D subcutaneous fat imaging and reconstruction.
This is a randomized, double-blinded study of three doses of MSDC-0602K or placebo given orally once daily to subjects with biopsy proven NASH with fibrosis and no cirrhosis.
The primary objective of this study is to evaluate the safety and tolerability of selonsertib, firsocostat, cilofexor, fenofibrate and/or Vascepa® in adults with nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH).
Background: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome, which is one of the major risk factors of coronary heart disease (CHD). CHD is the most important manifestation of atherosclerosis, because of its immense morbidity and mortality. Transient elastography (TE, Fibroscan®) including the currently developed controlled attenuation parameter (CAP) is a non-invasive method for evaluation of liver fibrosis and steatosis, which is already implemented in routine care of patients with NAFLD. Hypothesis: The use of TE with CAP as screening for NAFLD might be an easy tool for risk assessment for CHD. Methods: Patients scheduled for routine coronary angiography will be screened for manifestation of NAFLD by TE including CAP, conventional ultrasound, clinical and laboratory parameters. Patients will be stratified for the presence of CHD based on the angiography results and correlation analysis with liver fat content will be performed. NFALD screening will be validated in a subgroup by MR-based measurements.
To study the frequency of obstructive sleep apnea (OSA) and continuous positive airway pressure (CPAP) treatment response in patients with non-alcoholic fatty liver disease (NAFLD). It is hypothesized that CPAP treatment may improve the activities of NAFLD in those with concomitant OSA. A screening study for OSA followed by a randomized controlled trial of patients with biopsy proven NAFLD being followed up at the hepatology clinic. Home sleep study, Epworth sleepiness score (ESS), paired proton magnetic resonance spectroscopy (MRS), transient elastography by fibroscan, serum cytokeratin-18 fragment, liver function tests and liver biopsy (only for those with fibroscan evidence of advanced liver fibrosis). Patients with confirmed symptomatic OSA will be randomized to receive auto CPAP or subtherapeutic CPAP as control over 6 months. Primary outcome: changes in intrahepatic triglyceride content (IHTG) measured by proton-MRS after 6 months of auto CPAP versus subtherapeutic CPAP.
Fatty liver disease is an increasing problem in overweight and obese young adults. The purpose of this study is to test the effect of growth hormone on liver fat in obese young adults ages 18-29y with increased liver fat.
SGLT2 inhibitors have been proven to be effective in several preclinical rodent models of non-alcoholic fatty liver disease (NAFLD). Using a choline deficient diet to recapitulate some of the histological features of human non-alcoholic steatohepatitis (NASH), it was found that 5 weeks of SGLT2 inhibition led to significant reductions in hepatic triglyceride content and improved markers of liver fibrosis. Similarly, 4 weeks of treatment in obese mice led to improved glucose tolerance, reduced hepatic steatosis and reduced markers of liver oxidative stress in a dose dependent manner. These findings corresponded with an improvement in traditional liver function tests including the aminotransferases (ALT and AST). The widely used antidiabetic agent metformin has been shown in rodent models to increase hepatic insulin sensitivity and lower liver fat content which is in contrast to the findings in humans where metformin increases hepatic insulin sensitivity, reduces body weight but does not decrease liver fat content. The reason for the discrepancy between the animal and human studies, with regards to liver fat content remains unclear. The investigators hypothesise the following: - SGLT2 Inhibitors have the potential to decrease lipid accumulation in the liver through reduced de novo lipogenesis (DNL) - There will be no decrease in endogenous lipid synthesis (DNL) with metformin and thus no change in liver fat content. There are two arms to this study. - Arm 1: x10 participants with poorly controlled type 2 Diabetes (T2DM) who have been recommended to start an SGLT2 inhibitor called dapagliflozin will be recruited. - Arm 2: x13 participants with insulin resistance who have not yet started any diabetic medication will be recruited and will be prescribed metformin at standard clinical doses. The two arms will run in parallel and all participants will undergo identical investigations before and after 3 months of treatment with either dapagliflozin or metformin. Investigations will include liver magnetic resonance imaging/spectroscopy, fat biopsy, fat microdialysis sampling, two-step hyperinsulinaemic euglycaemic clamp, breath sampling and stable glucose and palmitate isotope infusions. The investigators aim to show that SGLT2 inhibition decreases liver fat whereas we aim to demonstrate why liver fat remains unchanged in humans, treated with metformin. These data will provide the first evidence for the use SGLT2 inhibitors in NAFLD, and will be highly informative for the design of future clinical studies. Moreover, the data gained from the metformin arm of the study will provide the first mechanistic evidence in humans of the effects of metformin on hepatic fatty acid metabolism.