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OSA rises the possibility of a person becoming insulin resistant and diabetic. The investigators will do this by comparing glucose metabolism in people with OSA and those that do not have OSA, as well as analyzing the effects of treating OSA by providing continuous positive airway pressure or simply oxygen throughout the night, and others that do not. Knowing the primary cause of Obstructive Sleep Apnea and pathophysiological factors responsible for OSA-related metabolic abnormalities may help with the development of potentially new therapeutic strategies for adults in improving OSA and related comorbidities.
Source link: https://clinicaltrials.gov/ct2/show/NCT03408613
Objective: To determine the potential mechanism by which high saturated fat intake disrupts normal skeletal muscle metabolism. No information has been found on the physiological basis for skeletal muscle metabolic inflexibility. Gut permeability and blood endotoxin has been gaining attention lately in the pathology of metabolic derangements related to obesity and T2D. Both at the whole body and tissue level, Rodent studies have established direct links between the gut microbiome and metabolic disease, as well as associations between elevated blood endotoxin and metabolic dysregulation. Increased blood endotoxin and single meals have been shown to raise blood endotoxin, but there are no studies in humans that high fat feeding results in metabolic endotoxemia. In addition, there are no reported correlations between gut permeability, metabolic endotoxemia, and skeletal muscle metabolic function in humans. We're suggesting that we use a model of acute high fat feeding in healthy humans to investigate the relationship between gut function, blood endotoxin, and skeletal muscle pro-inflammatory signaling and metabolic adaptability. We will begin with a two-week lead-in period, during which participants will be introduced to healthy eating habits and high saturated fat feeding, followed by five days of high saturated fat intake. The high saturated fat feeding period will consist of cooked meals that are isocaloric to a regular diet with a macronutrient content of 50% fat, 35% carbohydrate, and 15% protein.
Source link: https://clinicaltrials.gov/ct2/show/NCT02328235
HERG mutations cause LQTS caused by HERG mutations is the second most common form of LQTS. Following oral glucose intake in humans, the investigators wish to investigate the effects of Kv11. 1 blockade on incretin and insulin secretion, and blood glucose levels. Hypothesis of this study The investigators speculate that a Kv11. 1 blockade will raise the metabolic response of serum insulin and GLP-1 to a 6-hour 75 g oral glucose tolerance test in healthy people. The participants will have a continuous glucose monitor before and during the exam, and a glucose questionnaire will be filled out on the day of the test. Group A will be first given the active drug known to have Kv11. 1 blockade effects three days before the test visit 1; then, after a 3 weeks washout period, be given a placebo drug prior to test visit 2, and then, group B, which follows a three-day washout period, will be randomly assigned to either group A or B by a qualified unblinded individual from the University of Copenhagen's Department of Biomedical Sciences, University of Copenhagen, will first be ade pharmac ade effects, be randomized drug known to have Kv11. 1 blockade pharmac test visit to either group A or B, receives, a test visit to test visit to test visit 2 will be a test visit 2nd. The placebo drug will be first administered 3 days before test visit 1 and then receive the active drug for the first time during test visit 2. Test visit 1: Receive the test visit 1 and be instructed to orally administer the medication every morning at 6. 00 AM 3 days prior to and the same morning as the test visit. Participants will arrive and have a CGM monitor installed 4 days before to the test visit 2 for up to seven days, orally administer the drug every morning at the same time3 days before and during the same morning as the test visit 2’s two participants. Test visit 2 : Same tests as described for Visit 1. Participants must have orally administered the study drugs three days before and at the same morning as the test visits were carried out simultaneously. Participants are not allowed to take paracetamol 24 hours before testing visits. The trial participant's number is matched with the list, which reveals which group the participant is selected. After the Last Patient Last Visit, the unblinded individual will conduct any unblinding of the trial participants. The subject and the biological data obtained from the subject will be identified by subject number and trial identification number, according to data processing's reports. Laboratory results will be securely transferred from the lab's performing clinical studies and will be archived in secured hard drives with backup options. The electronic records will be considered source data. In cases where laboratory data is sent via non-secure electronic networks, the information will be encrypted during transfer. Anamnesis, weight and height measurements, and ECG are among the Case Report Form's most comprehensive reports.
Source link: https://clinicaltrials.gov/ct2/show/NCT03868657
Non-alcoholic fatty liver disease is the most common hepatic disease in the Western world, and it is a leading cause of liver-related morbidity and mortality. By using a metabolomics-based dynamic paradigm, we recommend a pilot study to explore patients with NAFLD's metabolic response to a standard food challenge. In this research, we will recruit 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 assessment of metabolic rates, and will be treated to a liquid mixed meal containing around 30% of daily caloric intake for a period of 15 minutes.
Source link: https://clinicaltrials.gov/ct2/show/NCT02520609
The study reveals two specific objectives: if blocking enteric neuronal signaling will change: a circulating supply of nutrient substrates and shrouding of hormones that control nutrient metabolism; and b glucose and fatty acid absorption, production, and utilization. Before the infusion of glucose and oleic acid into the duodenum, the topical anesthetic benzocaine will be infused into the duodenum. Infusions of naso-intestinal feeding tube will solve the confounding effects of gastric emptying on metabolic reactions to a meal. If enteric neural signals control appetite, Aim 2 will determine if enteric neural signals control appetite.
Source link: https://clinicaltrials.gov/ct2/show/NCT02537314
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