Active clinical trials for "Fatty Liver"

People with liver disease report difficulties with attention and problem-solving skills. Diet plays an important role in the development of liver disease and/or pre-diabetes. The purpose of this study is to examine whether participation in a brief diet intervention (up to 3 weeks) can improve brain and liver health and function.

Non-alcoholic fatty liver disease (NAFLD) is a multifactorial disease affecting a quarter of the world population. Pathological accumulation of fat, into the hepatocytes, is the first hit and is due to altered hepatic and extrahepatic lipogenesis, lipolysis and lipophagy of the large lipid droplets. Lipophagy plays a key role in the onset of NAFLD, in the autolysosomes, small droplets of fat are catabolized by Lysosomal Acid Lipase (LAL) enzyme which hydrolyzes cholesterol esters and triglycerides forming cholesterol and free fatty acids. Our research group demonstrated that, subjects affected by NAFLD, present a reduced enzymatic activity either compared to patients with chronic liver disease of different etiology, but comparable staging, either compared to healthy control subjects. Leukocytes are the main site of enzymatic activity in the blood, however, our research group has shown that it can also be detected inside the platelets, demonstrating how the LAL activity can be exchanged between cells. Furthermore, our group has shown, for the first time, how the intracellular enzymatic activity is reduced, independently of the platelets and leukocytes count and progressively from chronic liver disease up to cirrhosis. Among factors which contribute to altered lipid metabolism, the genetic predisposition to the accumulation of hepatic fat must be counted. Several variants of genes that code for proteins implicated in the digestion or storage of fats, are involved. In this study were considered: patatin-like phospholipase domain-containing 3 (PNPLA3), Transmembrane 6 superfamily 2 (TM6SF2) and 17β-Hydroxysteroid dehydrogenase type 13 (HSD17B13). The rs738409 variant (C> G, p.I148M) of the PNPLA3 gene consists of a protein in which the catalytic site is not entirely accessible to the substrate which, consequently, accumulates in the storage site. This variant is commonly found in NAFLD subjects and it has been widely reported how the variant carriers progress faster towards severe disease (steatohepatitis) than wild type subjects. The TM6SF2 gene encodes a membrane transporter involved in the triglycerides movement, the rs58542926 (C> T E167K) variant has been associated with an increased predisposition towards liver fibrosis in NAFLD subjects. This is likely due to the loss of protein function resulting in hepatic retention of triglycerides and cholesterol. Unlike PNPLA3 and TM6SF2, the rs72613567 (TA> TAA) variant of the HSD17B13 gene has a protective effect against NAFLD progression. It is characterized by a protein loss of function that protects against chronic liver damage and mitigates the progression of the disease although how the protective effect occurs is still under study. Due to the multifactorial etiology of the disease, to the need of carrying out a targeted surveillance in predisposed genetic subjects and, in order to prevent NALFD progression towards severe pathological forms characterized by an increased mortality, in this study, 316 subjects will be enrolled. They will be divided as follows: Italian Caucasians, aged> 18 and <70 years, with non-cirrhotic NAFLD and carriers of the PNPLA3 I148M variant, and, 158 Italian Caucasian subjects, aged> 18 and <70 years, with non-cirrhotic NAFLD and carriers of the wild type allele. The following exclusion criteria will be considered: any type of malignant disease in the past 5 years, any type of inflammatory or autoimmune disease, corticosteroids for systemic use, any type of drug that may affect body weight or body composition, insufficiency kidney (GFR <90 mL / min), heart failure (NYHA classes II-IV), any type of liver disease rather than NAFLD, excessive alcohol intake (> 140 g / week for men and 70 g / week for women), participation in a weight reduction program in the past 3 months, bile salts, cholestyramine in the last 6 months prior to enrollment, previous cholecystectomy, gallbladder disease. Peripheral blood will be withdrawn in order to measure haematic lipids (total cholesterol and fractions, triglycerides), total blood LAL activity, to perform genetic analysis and finally to evaluate lipase activity into the platelets. Hepatic elastography will be also executed, in 100 patients, according to the presence/absence of the PNPLA3 variant, in order to weigh up the genetic predisposition on NAFLD development or progression Finally, in subjects who present a lipase activity 30% lower than the normal value (0.88 ± 0.38 (mean ± SD), the methylation of the LIPA promoter will be studied.

Non-alcoholic fatty liver disease (NAFLD) has become a major health problem worldwide with an increasing prevalence ranging from 13% in Africa to 42% in South-East Asia. The term NAFLD includes a variety of diseases, ranging from liver fat deposition in more than 5% of hepatocytes (steatosis-non-alcoholic fatty liver (NAFL)) to necroinflammation and fibrosis (non-alcoholic steatohepatitis (NASH)), which can progress into NASH-cirrhosis, and eventually to hepatocellular carcinoma 1 Lifestyle modifications remain the cornerstone of NAFLD treatment, even though various pharmaceutical interventions are currently under clinical trial. Among them, sodium-glucose co-transporter type-2 inhibitors (SGLT-2i) are emerging as promising agents. Processes regulated by SGLT-2i, such as endoplasmic reticulum (ER) and oxidative stress, low-grade inflammation, autophagy and apoptosis are all implicated in NAFLD pathogenesis 2 In non-DM patients, only a small single center study exists which studied 12 patients under dapagliflozin and 10 patients under teneligliptin, a DPP4 inhibitor, for a total of 12 weeks, showing that after this intervention period, serum transaminases were decreased in both groups, while in the dapagliflozin group, total body water and body fat decreased, leading to decreased total body weight.3

This study aims to evaluate the possible beneficial effect of empagliflozin versus pioglitazone on non-diabetic patients with non-alcoholic steatohepatitis (NASH). This study will be a randomized, comparative parallel study. The study will be conducted according to the ethical standards of Helsinki declaration in 1964 and its later amendments. The study duration will be 24 weeks. The patients will be randomized into two groups: Group 1: (Pioglitazone group; n=28) which will receive 30mg/day pioglitazone for 24 weeks. Group 2: (Empagliflozin group; n=28) which will receive 10mg/day empagliflozin for 24 weeks.

Non-alcoholic fatty liver disease (NAFLD) is a liver disease, caused by storage of fat in the liver. The most-important risk-factors are being overweight, and disorders in sugar and cholesterol handling of the body. On average does around 30% of the population worldwide have any signs of fatty liver. Most people will not get severe complaints as a result of their fatty liver. But in some of them, the fat storage will lead to hepatitis. This causes damage to the liver which can eventually lead to scarring of the liver, and in some patients to cirrhosis. This possibly can cause liver failure, liver cancer, an several complaints which reduce the quality of life. There are several tests which can help in detecting scarring of the liver. However, the scientific world still does not know well enough which test works best and if they perhaps might work better if they are used together. In this study these questions will be investigated in order to design a care path which does several tests consecutively. The goal is that this will make it possible to easily detect a severely diseased liver and that this will eventually help to detect patients earlier so they can be treated earlier and complications of the disease might be reduced. Moreover, is the goal that this study will lead to a decrease in unnecessary referrals to a hepatologist, resulting in a reduction in invasive diagnostic interventions. Hospital specialists who think that their patient might be at risk for advanced liver disease, can refer a patient to this study. Participants will go to the hospital for one study visit where several tests will be done which are designed to detect liver scarring. Depending on the results, a participant will be referred to a hepatologist for more extensive diagnostics or referred back to the referring specialist with advice for management of the disease.

This is a Phase 2a, randomized, double-blind, placebo-controlled, parallel group, multiple arm, multicenter study of 3 different doses of HPG1860 versus placebo in subjects with biopsy-confirmed or phenotypic NASH.

TARGET-NASH is a longitudinal observational cohort study of patients being managed for NASH and related conditions across the entire spectrum NAFLD in usual clinical practice. TARGET-NASH is a research registry of patients with NAFL or NASH within academic and community real-world practices maintained in order to assess the safety and effectiveness of current and future therapies.

The primary objective of the study is to compare the changes in serum ALT level among patients with non-alcoholic steatohepatitis (NASH) following 3-month treatment of 800 mg SNP-610 or the placebo. The secondary objectives will be to compare the changes in liver fat fraction, other liver function tests, cytokeratin-18 (CK-18) fragment level and adverse event / serious adverse event rates among the interventional and placebo arms.

Obesity is an epidemic in the US. With progression of obesity, Nonalcoholic steatohepatitis (NASH) has been a growing public health issue. Presently there is no cure for NASH.Prevention of progression of fibrosis in NASH is crucial, as they are at a high risk for cirrhosis and may need liver transplant. Recent studies have shown that blocking blood vessels to a particular portion of the stomach (bariatric or left gastric artery embolization) can temporarily decrease levels of the appetite inducing hormone ghrelin, and result in weight loss.The purpose of this study is to determine if Left gastric artery embolization (LGAE) in patients with obesity and NASH leads to clinically significant weight loss with improvement of NASH.

Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide and is a major cause of cirrhosis and liver cancer in Western countries. Because of its close association with obesity and diabetes, most patients are seen by primary care physicians and endocrinologists rather than hepatologists. Previous studies have shown that NAFLD is under-recognized outside specialist settings. As a result, many patients are undiagnosed and not receiving specific treatments. With this background, we aim to test the hypothesis that the use of simple fibrosis scores as part of a diabetes complications screening program followed by electronic reminder messages is more effective than usual care in prompting physicians to correctly identify patients with suspected NAFLD and advanced liver fibrosis for specialist referral or further liver assessment. Our secondary aim is to test the hypothesis that the use of fibrosis scores and electronic reminder messages can increase the number of patients with confirmed diagnosis of advanced liver fibrosis.