View clinical trials related to Fatty Liver, Nonalcoholic.
Filter by:This study was conducted to investigate the effects of daily supplementation of fermented ginseng powder on improvement of Liver function.
Excessive fat in the liver, in absence of high alcohol consumption, is diagnosed as non-alcoholic fatty liver (NAFL). NAFL prevalence is as high as 50-70% in obese people and is associated with impairments in metabolic health, e.g. insulin resistance. Not only the amount, but also the composition of the fat stored in the liver appears to be linked to health outcome measures, such as insulin resistance, but this evidence comes mainly from animal studies. Since fat composition has been linked to health outcome measures, it is important to understand what determines the fatty acid composition of liver fat. De novo lipogenesis (DNL) and adipose tissue fat composition are factors that could determine liver fat composition. Since the end product of DNL are saturated fatty acids and as the majority of fatty acids in the liver originate from adipose tissue, both may influence hepatic fatty acid composition profoundly. Here, our primary hypothesis is that DNL is associated with the relative amount of saturated fatty acids in the liver in overweight/obese humans differing in liver fat content. Furthermore, we hypothesise that adipose tissue fat composition is associated with liver fat composition and that liver fat composition is associated with liver, muscle and whole body insulin sensitivity in overweight/obese humans differing in liver fat content. To this end, liver fat composition, adipose tissue fat composition, DNL and insulin sensitivity will be measured in overweight/obese participants differing in liver content.
The aim of this study is to evaluate the effects and safety of a dietary supplement, Zataria multiflora Boiss (Shirazi's Thyme) in the treatment of non alcoholic fatty liver disease (NAFLD).
The main aim of the study is to determine if an oral supplementation of the LCS has a beneficial effect by itself or even enhances the beneficial effects of a moderate life-style intervention on the progression of NAFLD in humans.
HMG co-A reductase inhibitors, commonly called statins, are an effective treatment for dyslipidemia and atherosclerotic heart disease with proven mortality benefit. While the lipid-lowering effects of statins are well-known, other metabolic effects, including effects on glucose tolerance and ectopic fat distribution, are less completely understood. Recent studies have shown that some statins may increase the risk of diabetes. Further, research has suggested that statins may have some benefit in nonalcoholic fatty liver disease (NAFLD), a condition associated with obesity that includes increased fat in the liver (steatosis) and, in some cases, inflammation and hepatocellular damage (steatohepatitis). Pitavastatin, approved by the United States Food and Drug Administration (FDA) in 2009, is the most recent statin to enter the market. Unlike most statins, pitavastatin is not primarily metabolized through cytochrome P450 (CYP450), and thus has reduced potential for interactions with other medications that are metabolized by CYP450. Previous studies have suggested that pitavastatin may be neutral to glucose homeostasis and may improve hepatic lipid. Neither of these effects has been proven definitively, however, and the current proposal aims to characterize in detail the effects of pitavastatin on glucose homeostasis, hepatic steatosis, and steatohepatitis.
There is a significant association between autonomic dysfunction and symptoms experienced by NAFLD patients mediated by increased systemic inflammation and insulin resistance, resulting in deteriorating quality of life of affected patients; fatigue and other symptoms drive worsening autonomic dysfunction in these patients. We aim to describe the severity of autonomic dysfunction (AD) in non-alcoholic fatty liver disease (NAFLD) and the relationship of AD to symptoms experienced by NAFLD patients (such as fatigue, chronic pain, depression, sleep disturbance, and cognitive dysfunction), and to the quality of life of NAFLD patients. We also hope to examine the impact of systemic inflammation and insulin resistance as mediators of manifestations of AD and symptoms experienced by NAFLD patients.