View clinical trials related to Fatty Liver.
Filter by:Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease, ranging from pure steatosis to non-alcoholic steatohepatitis and ultimately to liver cirrhosis. In order to study the association between NAFLD and nephrolithiasis while minimizing the confounding effect of metabolic syndrome, we investigated the impact of different degrees of NAFLD severity on potential risk factors for stone formation.
The current study aim was to conduct placebo-controlled randomize clinical trial to assess the short-term efficacy and safety of postbiotics on hepatic fat content as measured by biochemichal hepatic steatosis indeces, serum lipid profile, transaminases activity and chronic systemic inflammatory markers in MASLD patients. The study will include 3 periods. Screening period of up to 1 weeks to assess the eligibility to inclusion/exclusion criteria. Treatment period for 3 month where the participants will receive a twice daily oral dose of postbiotics (cell lysate and DNA fragments of the probiotic strain L. rhamnosus DV - NRRLB-68023) at the assigned dose of 100mg or placebo in capsules. During this period monthly phone contacts will be done for assessment of compliance and safety concerns. Follow-up period of up to 3 month.
Background: Non-alcoholic steatohepatitis (NASH) is an advanced form of non-alcoholic fatty liver disease (NAFLD) that can precipitate to advanced fibrosis and leads to cardiovascular morbidity and mortality. Many patients with type 1 diabetes mellitus (T1DM) had histological evidence of steatosis and met the histological criteria for NASH. Matrix metalloproteinase-14 (MMP-14) is a type 1 transmembrane proteinase expressed in liver fibrosis and is involved in the development of atherosclerosis and cardiovascular disease. Hepatic dipeptidyl peptidase-4 (DPP-4) expression in NAFLD may be directly associated with hepatic lipogenesis and liver injury. Some studies showed the beneficial effect of dipeptidyl peptidase-4 (DDP-4) inhibitors in NAFLD/NASH for their role in improving hepatic glucose metabolism. Vildagliptin, a DPP-4 inhibitor, could be promising therapeutic agents for NAFLD/NASH. To the best of our knowledge, no previous study assessed the role of DPP-4 inhibitors in adolescent patients with T1DM and NASH. Objectives: This randomized-controlled clinical trial assessed the impact of the oral DPP-4 inhibitor, vildagliptin, as an add-on therapy on NASH in adolescents with T1DM as well as its effect on glycemic control, lipid profile, MMP-14 levels and CIMT as a marker for subclinical atherosclerosis. Methods: This study included 60 adolescents with T1DM and NASH with a mean age 15.6 ± 2.08 years and disease duration ≥ 5 years. Forty age- and sex-matched healthy subjects with a mean age 14.9 ± 3.2 years were enrolled as healthy controls to compare MMP-14 levels. T1DM patients were randomly assigned to receive oral vildagliptin (50 mg daily) with lunch meal for six months or not. Fasting and 2 hours post-prandial blood glucose levels, HbA1c, liver function tests, fasting lipid profile, hepatic steatosis index and triglyceride glucose (TyG) index were assessed. MMP-14 levels were measured by enzyme-linked immunosorbent assay among all patients and healthy controls. CIMT was assessed using Doppler ultrasound and transient elastography with controlled attenuation parameter (CAP) was performed to assess liver stiffness and steatosis stage.
The purpose of this clinical trial is to investigate which exercise regimen is more effective in improving non-alcoholic fatty liver disease (NAFLD) in a young population. The primary questions it aims to answer are: Does aerobic training, resistance training, or a combination of both help improve liver function and glycemic and lipid parameters in NAFLD patients? Which of these three exercise regimens is more effective in improving the aforementioned parameters? Is the improvement in liver function related to bile acid metabolism? Participants will: Engage in physical exercise 4-5 times per week for two consecutive months, following a predefined exercise regimen. Have blood samples collected to test for glucose, lipids, liver function, and other parameters before starting the exercise program and after two months of completing the regimen.
- Objectives: Primary objective_To evaluate the safety and tolerability after single oral administration of the investigational product (IP), J2H-1702 in healthy female subjects. Secondary objective_To evaluate the pharmacokinetics (PK) and pharmacodynamics (PD) characteristics after single oral administration of the IP, J2H-1702 in healthy female subjects.
1. Research Purpose: To evaluate the safety, tolerability, pharmacokinetic/pharmacodynamic properties of J2H-1702 (a candidate for treatment of non-alcoholic steatohepatitis) in healthy men. 2. Design: A dose block-randomized, double-blind, placebo controlled, single- and multiple dosing, dose-escalation phase 1 clinical trial
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. It comprises a wide spectrum of disorders that range from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis, related cirrhosis, and even hepatocellular carcinoma (HCC).
Several controlled interventional studies have shown that there is a close correlation between cholesterol reduction and cardiovascular risk; in fact, reductions in serum levels of total cholesterol and low-density lipoprotein cholesterol (LDL-C), obtained through lifestyle modification or specific drugs, result in reductions in the incidence of major coronary events. The effectiveness of these interventions has been demonstrated both in subjects in primary prevention and in subjects in secondary prevention. Based on this evidence, the National Cholesterol Education Program (NCEP) has defined in the ATP III report the target values of LDL-C to be reached with interventions on food and / or pharmacological habits to perform an effective cardiovascular prevention. Although the atherogenic action of hypercholesterolemia is largely attributable to a direct damage exerted on vascular endothelium, recent studies suggest that the activation of a low-grade systemic pro-inflammatory state, typical of the patient with cardiovascular risk factors, does also play a role in the determinism of endothelial damage and atheroma degeneration of the arteries. It is believed that this systemic inflammation, as documented by the determination of some humoral signs of inflammation (e.g. C-reactive protein, interleukin-6, tumor necrosis factor-α), may further contribute to an increase of cardiovascular risk. The inflammatory state can modulate the atherosclerotic process at various levels, determining endothelial activation, promoting leukocyte chemotaxis in the sub-intimal space of the arterial wall and therefore the formation of an atheromatous plaque rich in inflammatory cells; the latter represents the lesion responsible for the vast majority of the coronary and cerebrovascular events observed in subjects with cardiovascular risk factors.
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease globally, with an estimated prevalence of approximately 15 to 30%. The incidence of NAFLD is even higher, reaching up to 58%, in individuals who are overweight or obese. The pathogenesis of NAFLD is complex and not fully understood. The metabolism of carbohydrates contributes to the development of NAFLD, as it increases the enzymatic activity of lipid synthesis in the liver, depleting adenosine triphosphate (ATP) rapidly and causing stress on mitochondria and endoplasmic reticulum. The multifunctional protein Glycine N-methyltransferase (GNMT) plays a regulatory role in liver carbohydrate metabolism, and its expression is downregulated in the liver tissues of NAFLD. While weight loss and lifestyle adjustments are helpful in controlling NAFLD, effective pharmacological or healthcare interventions for NAFLD patients are currently lacking. Insulin resistance is crucial in the pathogenesis of NAFLD, suggesting that drugs improving insulin sensitivity, such as metformin, might have therapeutic effects. However, recent large-scale clinical trial results have not supported this hypothesis. Investigators propose that the mitochondrial inhibitory effects of metformin may be related to this discrepancy, and the negative effects may be reversed through food containing substances promoting GNMT gene expression, such as Ganwei (as know as "HepatoKeeper"). Preliminary animal experiments also show that the combined use of metformin and GNMT enhancers effectively eliminates liver lipid droplet accumulation and improves liver inflammation in a NAFLD mouse model, surpassing the effects of either drug used alone. Based on these findings, our team designed the medication treatment group for this clinical trial, aiming to investigate whether the combination of Ganwei and metformin produces a synergistic effect in humans. Ganwei compound herbal extract capsules contain extracts from natural foods such as Schisandra chinensis, Paeonia lactiflora, and Punica granatum. Among them, Paeonia lactiflora is known to contain components that enhance GNMT expression. Animal and cell experiments have demonstrated its potential for repairing liver damage and inflammation. This trial aims to assess the impact of orally administering Ganwei compound herbal extract capsules on participants and evaluate its effects on fatty liver, liver fibrosis, and metabolic indicators.
The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing with obesity, and it is believed that ongoing inflammation in obesity and alterations in the enterohepatic axis contribute to this process. This study aimed to determine the role of fecal calprotectin (FCP) as an inflammatory biomarker in course of obesity and NAFLD.