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Patients who are enrolling in the program will either have had their liver biopsy or liver biopsy as part of their medical care as determined by their physician, and will not be getting biopsies solely to be enrolled in the study.
Source link: https://clinicaltrials.gov/ct2/show/NCT02754037
Non-alcoholic fatty liver disease and its progressive form, non-alcoholic steatohepatitis, is the leading causes of liver disease and are closely linked to obesity, diabetes, and metabolic syndrome. Although NAFLD reflects disordered energy metabolism in the liver, no data exists regarding the human liver's reaction to a meal's acute caloric load. In patients with steatosis, we now hypothesize a spillover effect, wherein NASH patients have an impairment of the hepatic ability to recite the amount of FA to triglycerides, resulting in the accumulation of lipotoxic intermediary metabolites. This study seeks to determine the hepatic response to an acute oral carbohydrate load; and to determine which baseline measurements can predict NAFLD patients's clinical responses to a course of semaglutide, a novel GLP-1RA. The non-randomized, single-center, pilot exploratory research in which up to 32 participants with NAFLD or NASH will undergo two liver biopsies, one in the fasting state and one in the fasting state, and the other in the second hour after an oral 75g glucose load was determined. All subjects will be monitored with semaglutide for 30 weeks, and their medical response will be determined by ALT and 1H-Magnetic resonance spectroscopy as well as a final liver biopsy. The human hepatic reaction to a meal has never been investigated at the tissue level, and this report is expected to produce important data and clarify some of the basic questions regarding insulin resistance mechanisms.
Source link: https://clinicaltrials.gov/ct2/show/NCT03884075
Non-alcoholic fatty liver disease is the most common hepatic disorder in the Western world, and it is a leading cause of liver disease and mortality. We recommend a pilot study to examine patients with NAFLD's digestive response to a standardized food challenge by adopting a metabolomics-based dynamic paradigm. This research will enroll up to 50 patients with NAFLD and compare them to 12 controls with metabolic syndrome without NAFLD and 12 healthy controls. Following an overnight fast, participants will be placed in a metabolic chamber for continuous monitoring of metabolic rates, and will be given a liquid mixed meal containing around 30% of daily caloric intake for a period of 15 minutes. The results of the study may help identify novel metabolic markers of disease and uncover new signaling pathways unique to NAFLD that are primarily under fed state conditions.
Source link: https://clinicaltrials.gov/ct2/show/NCT02520609
Patients with pituitary GH deficiency have a higher risk of NAFLD and non-alcoholic steatohepatitis than the general population, and GH replacement in these patients reduces liver damage. The aim of this research is to see if growth hormone therapy will reduce liver fat concentration in young adults with more than 5% liver fat measured by magnetic resonance spectroscopy.
Source link: https://clinicaltrials.gov/ct2/show/NCT02726542
In children aged 8 to 20 years old, the FIND trial will be a single-centre, placebo-controlled trial comparing the effects of 6 months of fructo-oligosaccharide supplementation versus placebo on hepatic fat content, hepatic stiffness, metabolic function, and body composition in children aged 8-17 years old. Assessments including MRI measurements of hepatic fat and hepatic stiffness, anthropometry and pubertal status questionnaires, and other research such as body composition by dual energy X-ray absorptiometry, fasting lipids, blood glucose, and oral-glucose tolerance tests will be conducted by REDCap software will be conducted; and randomization will be performed via REDCap software. In order to randomly select sixty participants for the intervention phase, eighty participants will be eligible for baseline analysis. Each day, participants will be consuming one packet of FOS or placebo. FOS or placebo therapy will be available for six months, with research visits being conducted at baseline evaluation, 3 months, and 6 months.
Source link: https://clinicaltrials.gov/ct2/show/NCT05480696
Simple steatosis is the accumulation of lipids in more than 5% of hepatocytes, but without treatment, up to 5% of patients with simple steatosis to steatosis is likely to liver cirrhosis and/or hepatocellular carcinoma. 2,3 Epidemiology b. k. a MAFLD is a drug induced by obesity, dyslipidemia, and type 2 diabetes. 9,10 Pharmacological and non-pharmacological treatment in MAFLD Several studies show that MAFLD patients with ocular steatosis are also linked to ischemic stroke, but not for MAFLD patients with type 2 diabetes, pioglitazone, and type 2 diabetes. 11, NASH patients without a single identifiable steatosis. Both aerobic and resistance exercise have significantly reduced intrahepatic lipid levels, according to exercise intervention studies in MAFLD. These benefits seem to be independent of exercise frequency and dose, according to 13. 13 The exact mechanisms by which exercise decreases intrahepatic lipid levels are not fully understood. Mechanisms involved in MAFLD's cardiovascular disease have recently been found to also influence cerebral blood flow altering cerebral hemodynamics in MAFLD participants. However, there are no studies examining the effect of lifestyle interventions on cerebral hemodynamics in patients with MAFLD, but it has been reported that in other pathologies with pathophysiological similarity with NAFLD, there have been positive changes in this regard. Patients with metabolic-associated fatty liver will have a reduced pulsatility index and resistance index, while the control group without a physical training program will have less compared to the control group without a physical training program. Secondary Aims To determine the effect of a physical training program for 16 weeks in patients with MAFLD compared to a control group on endothelial function determined by pulse rate testing in patients with MAFLD. Transient elastography in fatty liver disease related to metabolic dysfunction and skeletal dysfunction will determine the effect of a physical training program for 16 weeks compared to a control group on liver enzymes and the degree of liver steatosis and fibrosis. The effect of a physical fitness program for 16 weeks compared to a control group on patients with MAFLD's body composition is unclear. 36 samples out of 36 patients is 36 = 36: 36 Patients are needed to include 21 patients in each group considering a 20% loss if one of the two treatment groups is expected to see a difference in the middle cerebral artery or more between the two treatment groups.
Source link: https://clinicaltrials.gov/ct2/show/NCT05520697
According to statistics, Non-Alcoholic Fatty Liver Disease is the leading cause of chronic liver disease worldwide and impacts 25-30% of the population in Western countries. Cardiovascular disease is the leading cause of death in people with NAFLD, followed by extrahepatic malignancies and liver-related disorders. It is now widely accepted that liver fibrosis is a result of liver injury secondary to NAFLD, and it is a leading predictor of liver-related and total mortality in people with NAFLD. Numerous risk factors for fibrosis progression have been identified: age, hypertension, obesity, and type 2 diabetes are all typical risk factors for fibrosis progression. Cellular senescence has been proposed as a causal factor in the onset and progression of NAFLD and NAFLD-related liver fibrosis. Interestingly, metabolic dysregulation is thought to promote cell senescence in several tissues involved in NAFLD pathology, including liver, pancreas, and adipose tissue, contributing to metabolic dysregulation. Due to the fact that senescence in NAFLD-related fibrosis, desatinib plus quercetin may thus be a promising future therapeutic option to treat NAFLD-related fibrosis. We want to perform a double-blind controlled proof-of-principle research in which patients with NAFLD-related liver fibrosis will be treated with dieatinib plus quercetin for three weeks and a four-week medication-free period. Based on the long-term safety profile of these drugs and the high unmet medical need as there is no cure for NAFLD related liver fibrosis, patients with NAFLD-related liver fibrosis.
Source link: https://clinicaltrials.gov/ct2/show/NCT05506488
Patients from Alexandria Teaching Hospital, a General Organization for Teaching Hospitals and Institutes, will be recruited by Alexandria Teaching Hospitals and Institutes, among other potential users. Patients will be tested for insulin resistance using biochemical tests, aspartate aminotransferase, homeostasis model evaluation of insulin resistance, Hemoglobin A1C, Low-density lipoproteins, Triglycerides, liver fibrosis score, and complete blood count are among the patients' results. Adipocytes are able vascular adhesion molecule-1, soluble vascular cell adhesion molecule-1, and molecular tests will be performed on the patient.
Source link: https://clinicaltrials.gov/ct2/show/NCT05459701
Although fat intake has remained relatively steady, the marked rise in dietary fructose consumption supports the role of fructose in NAFLD and the metabolic syndrome. Although the reason for fructose-related liver injury is not well defined, fructose-related hepatic adenosine triphosphate depletion may play a role in liver injury, the cause for liver injury can not be identified. One major difference in fructose metabolism is the depletion of ATP and the reliance on adenosine monophosphate kinase to replenish ATP stores. KHK's high success in converting fructose to fructose-1-phosphate in the liver may lead to liver ATP depletion in the case of hepatic ATP depletion due to habitual fructose intake. Patients with NAFLD have 3-4 times more fructose than controls without liver disease, according to our researchers, as previously reported in animals. Fruitose has been linked to NAFLD disease progression in relation to increased fructose intake, which has been attributed to increased fructose intake. Our team has found that patients with biopsy-proven NAFLD have elevated mRNA expression of KHK in comparison to matched controls, in favor of our assertion that ATP depletion underlies liver injury in patients with NAFLD. ATP depletion in liver cells can perpetuate chronic liver disease by making fatty hepatocytes less active. Patients with cirrhosis and NASH in IV fructose infusion were significantly higher than in healthy controls, with elevated uric acid levels above the baseline level after IV fructose infusion. Fruit load modification in metabolic steps of hepatic metabolism in people with alcohol-related liver disease may be used effectively by 31P MRS, according to other investigators. In addition, IV fructose loading in cirrhotic patients leads to substantially higher ATP degradation and uric acid production in cirrhotic patients than in healthy controls. In accordance with our hypothesis, increased uric acid is an independent risk factor for NAFLD, and hyperuricemia in patients with NAFLD may be a surrogate marker of impaired liver function homeostasis. In Figure 1, the proposed protocol for fructose-related hepatic ATP depletion, NAFLD, NASH, and related hyperuricemia are shown as novel, innovative, scientifically rigorous, and addresses an important public health issue-the effect of fructose on the increasing epidemic of NAFLD.
Source link: https://clinicaltrials.gov/ct2/show/NCT01930123
Adding mindfulness to lifestyle changes for weight loss can contribute to fatty liver disease in particular and overall health and well-being in general, as well as general health and well-being by assisting in weight loss and maintaining a healthy lifestyle. Non-alcoholic fatty liver disease is a disease in which excess fat in the liver of people who drink little or no alcohol is present. Participants in this report will receive regular health care, but in addition, they may be required to enroll in a mindfulness-based stress reduction program for 8 weeks.
Source link: https://clinicaltrials.gov/ct2/show/NCT05130346
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