Active clinical trials for "Fatty Liver"

The purpose of this study is to evaluate the effect of Protandim on the degree of liver injury after one year of supplementation. Protandim is a nutritional supplement composed of the following 5 botanical extracts: Bacopa Moniera extract, Milk Thistle extract, Ashwagandha powder, Green tea, and Turmeric extract. Protandim is commercially available and can be purchased without a prescription. Our findings could lead to a better understanding of the role of oxidative stress and antioxidant therapy in NASH and may ultimately help improve patient care. Hypothesis #1: Protandim will lead to a significant improvement in NAS compared to placebo. Hypothesis #2: Protandim will lead to a significant decrease in serum markers of oxidative stress and liver chemistry tests. Hypothesis #3: Protandim will lead to decreased levels of TNF- α compared to placebo.

The primary aim of the study is the effect of spironolactone and vitamin E versus vitamin E on serum levels of adipokines 52 weeks post-treatment.

Trial Synopsis: Bovine Colostrum for patients with non alcoholic fatty liver disease (NAFLD). Design: This is a single-arm, open-label, before-and after exploratory trial of 30 days of Bovine Colostrum Powder (BCP) to improve NAFLD and the metabolic syndrome. Duration: 8 weeks per subject. Sample Size: 30 subjects. Population: Patients with biopsy proven NASH (NAS of > 4) and an ALT level of ≥ 30 (U/L). Regimen Study treatment will consist of BCP, three 1.2 g oral tablets (equivalent to 600 mg of BCP each) for 4 weeks, from cows immunized to insulin. Patients will be followed for safety monitoring for an additional 4 weeks.

This clinical study is designed to evaluate the safety of oral administration of the medical food Hoodia to patients with non alcoholic fatty liver disease. Oral administration of Hoodia is common in many western world countries for appetite suppression and as a food supplement or medical food used for dietary purposes. Nonalcoholic steatohepatitis or NASH is a common, often "silent" liver disease which affects about 2%-5% of Americans. NASH is strongly associated with the metabolic syndrome, diabetes type-2 and obesity and can lead to cirrhosis, HCC, liver transplantation or death.This clinical trial has been designed to assess the safety of short term oral administration of Hoodia to patients with NASH.

To assess whether reversal of fatty liver by moderate weight loss (8% of body weight) will lead to improvements in insulin sensitivity, which will be associated with changes in both glucose status and lipid profiles, in obese children and adolescents with fatty liver who have normal glucose or pre-diabetes.

To assess the safety and efficacy of betaine in patients with NASH on markers of disease severity such as liver histology, liver biochemistries, and health related quality of life.

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver condition frequently associated with type 2 diabetes (T2DM) and characterized by insulin resistance and hepatic fat accumulation. Liver fat may range from simple steatosis to severe steatohepatitis with necroinflammation and variable degrees of fibrosis (nonalcoholic steatohepatitis or NASH). Up to 40% of patients with NAFLD develop NASH in recent series. Risk factors for progression to NASH are unclear, but appears to be more common and progress more rapidly in older individuals, and in the presence of obesity and T2DM. Because the VA population in San Antonio, Texas, frequently combine these risk factors for NASH it was felt that a study targeting this very high-risk population was needed. This study will establish the long-term efficacy (primary endpoint: liver histology) and safety of pioglitazone for the treatment of VA patients with T2DM and NASH. All patients diagnosed with NASH will be offered lifestyle modification/weight loss (current standard of care) while being randomized to pioglitazone, vitamin E or placebo for up to 3 years. We believe that in such a high-risk population for complications from NASH, a substantial benefit may be expected from early detection and treatment. Specifically, the arms are: a) pioglitazone + vitamin E; b) vitamin E + placebo of pioglitazone; c) placebo of both. Patients are randomized to one of these 3 arms, and followed in a double-blind fashion for up to 18 months. Patients are then offered to continue into an open-label phase with pioglitazone + vitamin E or vitamin E alone for another 18 months.

The prevalence of NAFLD is 50-70% in obese people. A decrease of calorie intake and increase of physical activity are recommended as an effective approach for the prevention and treatment of NAFLD. However, the exercise model for NAFLD intervention is understudied. In the present study we aim to compare the effect of intensive and conventional exercise interventions on NAFLD.

This research is being done to examine: 1) how common obstructive sleep apnea (OSA) is in patients with non-alcoholic fatty liver disease (NAFLD), 2) whether the severity of OSA is related to the severity of NAFLD, and 3) whether treatment of OSA with continuous positive airway pressure (CPAP) improved NAFLD progression. OSA is a condition caused by repetitive collapse of throat tissue during sleep that leads to falls in oxygen level and sleep disruption. OSA can be caused by obesity, and especially by fat found in the neck and belly. NAFLD is a common disease linked to obesity. NAFLD is part of a disease spectrum, which can progress from steatosis (fatty liver) to nonalcoholic steatohepatitis (NASH), a progressive fibrotic disease, in which cirrhosis and liver-related death can occur. Recent evidence in patients with obstructive sleep apnea (OSA) indicates that OSA is associated with NASH. How common OSA is in patients with biopsy-confirmed NAFLD and the effect of OSA treatment with CPAP on NASH is unknown.

The primary goal of this study is to provide a better understanding of: 1) the pathogenesis and pathophysiology of non-alcoholic fatty liver disease (NAFLD) in obese subjects, and 2) the effect of marked weight loss on the histologic and metabolic abnormalities associated with NAFLD. The following hypotheses will be tested: obesity causes hepatic fat accumulation because of excessive fatty acid release from fat tissue and increased free fatty acid availability, increased hepatic (liver) fat content causes insulin-resistant glucose (sugar) production by the liver and altered liver protein synthesis, increased hepatic fat content causes increased lipid (fat) peroxidation, hepatic inflammation, necrosis and fibrosis, and marked weight loss improves NAFLD once patients are weight stable.