View clinical trials related to Fructose Intolerance.
Filter by:Hereditary fructose intolerance (HFI) is a rare inborn error of metabolism. Patients with HFI develop acute abdominal pain, nausea, vomiting, hypoglycemia and proximal tubular dysfunction upon consumption of a fructose containing food product. In rare cases, (prolonged) fructose consumption can even lead to liver and kidney failure. Patients with HFI are therefore treated with a lifelong fructose-restricted diet. Animal studies have shown that the clinical manifestations of HFI are abrogated upon inhibition of ketohexokinase (KHK), the enzyme that catalyses the first step in fructose metabolism. Recently, PF-06835919, a KHK inhibitor (KHKi), was developed as a new treatment for non-alcoholic fatty liver disease. The compound was well tolerated in several phase II clinical trials. It is hypothesized that PF-06835919 is also effective in patients with HFI.
Cardiometabolic diseases have been associated with high consumption of sweetened beverages. These products are responsible for the largest portion of the total consumption of fructose in the diet and it is suggested that excessive intake of this monosaccharide may contribute to the development of risk factors for these diseases due to differences in metabolism relative to glucose. However, there is a lack of data in the literature demonstrating the deleterious effects of excessive fructose consumption on vasodilation and whether aerobic training may be able to prevent or mitigate these damages in humans. Therefore, the aim of the study will be to verify the effect of 4 weeks of high fructose diet associated with aerobic training on uric acid levels and its influence on markers related to oxidative stress and vasodilatation. Twenty-one sedentary men and women, aged between 19 and 35 years, will be submitted to 4 weeks of intervention. In a randomized way, subjects will be divided into 3 groups: high fructose diet, high glucose diet and high fructose diet and exercise. Blood samples will be taken before, in the middle and after the intervention to verify the concentrations of uric acid, superoxide dismutase enzyme, thiobarbituric acid, nitrite / nitrate, lipid profile, glucose, insulin, C-reactive protein and endothelin-1. In addition, flow-mediated dilatation, insulin resistance index, pancreatic beta cell functional capacity index, oral glucose tolerance test, 24-hour blood pressure, heart rate variability and body composition will be analyzed. The comparisons will be performed through the Generalized Estimates of Equations, adopting the factors group and time. The Bonferroni post-hoc will be used to identify differences. The accepted level of significance will be 5%.
This study aimed to examine metabolic response to a short-term fructose enriched diet in carriers for hereditary fructose intolerance compared to controls. Effects of fructose coffees will be assessed in 7 healthy volunteers and 7 subjects with heterozygous mutation for ALDOB gene in a randomized, controlled, crossover trial.
Bloating, gas, pain and diarrhea are common complaints. Routine investigations are negative; these patients are labeled as IBS. In these patients, whether testing for carbohydrate malabsorption or small intestinal bacterial overgrowth (SIBO) is useful is unclear. Investigators aim to assess the prevalence of SIBO, fructose and lactose intolerance, the usefulness of breath tests, and predictive value of pre-test symptoms.
Background: High fructose intake increases blood lactate, triglyceride and uric acid concentrations. Uric acid may contribute to insulin resistance and dyslipidemia in the general population. In patients with hereditary fructose intolerance fructose consumption is associated with acute hypoglycemia, renal tubular acidosis, and hyperuricemia. Objective: We investigated whether asymptomatic carriers for hereditary fructose intolerance (HFI) would have a higher sensitivity to adverse effects of fructose than the general population. Design: Eight subjects heterozygous for HFI (hHFI; 4 males, 4 females) and eight controls received for 7 days a low fructose diet and on the eighth day ingested a test meal calculated to provide 25% of basal energy requirement containing labeled fructose (13C fructose 0.35 g/kg), protein (0.21 g/kg) and lipid (0.22 g/kg). Total fructose oxidation, total endogenous glucose production (by 6,6-2H2-glucose dilution), carbohydrate and lipid oxidation, lipids, uric acid, lactate, creatinine, urea and amino acids were monitored for 6 hours.
In this study we will investigate the expression of the fructose transport protein GLUT5 in the small intestine in patients with functional GI disoders and fructose intolerance compared to matched healthy controls.