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In the intensive care units, septic shock is both common and morbid. SIMD is related to stress-induced cardiomyopathies and biomechanistic characteristics characteristic of chronic heart failure traditionally attributed to a coronary disease. Dobutamine, a beta-adrenergic receptor agonist, is the inotrope drug recommended when cardiac index is too poor, often in association with a blend of alpha-beta agonists such as norepinephrine. Although a direct correlation between myocardial metabolism homeostasis and function is not established in normal circumstances, a compensatory equilibrium between fatty acid and glucose mitochondrial oxidations is a generally accepted term. In 50% of acute sepsis within the first 48 hours after patient admission, left ventricular systolic and diastolic dysfunctions were present in 50% of acute sepsis. Animal experimental models can mimic human sepsis and SIMD by injecting endotoxin or feces in the abdominal cavity, and with inflammatory cytokines, oxidative stress, nitric oxide, and neutrophils as potential aggressors. Ca2+ handling in aberrant during sepsis and contaminated with poor activation/phosphorylation and proteolytic cleavage, a major regulators, such as heart troponin I, is being absorbed by a significant regulator, such as heart troponin I. A decline of fatty acid oxidation in these conditions and in the heart is not necessarily compensated by increased glucose use. In 1987, Dhainaut et al became the first to demonstrate a change in the selection of energy fuels by myocardial tissue in septic shock patients. Which energy source is favored by cardiac mitochondrial dysfunction in acute septic shock with or without myocardial dysfunction in acute septic shock, with or without myocardial dysfunction vs non-septic CHF? Hypotheses: A myocardial positron emission tomography may help to visualize and quantify hearts in acute shock conditions related or not related to sepsis. Methods: 1: a case study of 4 groups of 8 patients in acute heart failure or with reduced ejection percentage compared to hemodynamic support; iii a group with evidence of SIMD in the first 48 hours: a systolic ejection fraction 45% or cardiac insufficiency with reduced ejection fraction 45%, iii a group in acute heart failure under hemodynamic assistance.
Source link: https://clinicaltrials.gov/ct2/show/NCT05202938
The effects of various food derived polyphenols on cardiovascular health are on cardiovascular health are on increasing demand. The aim of this investigation is to investigate the connection between polyphenol microbiota metabolism and cardiovascular health. Participants in the age range from 20 to 70 years old health overweight men and women. For three days, the participants will enjoy a polyphenol rich breakfast.
Source link: https://clinicaltrials.gov/ct2/show/NCT03573414
This research is designed to identify the key causes and mechanisms responsible for dysregulated glucose metabolism in people with OSA. The investigators will do this by comparing glucose levels in people with OSA and those that do not, as well as determining the effects of treating OSA by providing continuous positive airway pressure or simply oxygen during the night. Knowing the root cause of Obstructive Sleep Apnea and pathophysiological disorders associated with OSA-associated metabolic abnormalities may help establish potentially new therapeutic strategies for adults with the intention of reducing OSA and related comorbidities.
Source link: https://clinicaltrials.gov/ct2/show/NCT03408613
Objective: To determine the potential mechanism by which high saturated fat feeding disruptions normal skeletal muscle metabolism. The mechanism that causes skeletal muscle metabolic inflexibility is unknown. In the pathology of metabolic disorders associated with obesity and T2D, there has been increasing concern in the role of gut permeability and blood endotoxin. Both at the whole body and tissue level, Rodent studies have established direct links between the gut microbiome and metabolic disease, as well as links to elevated blood endotoxin and metabolic dysregulation. Increased blood endotoxin and T2D have been reported in humans, obese, and T2D can be blamed for increased blood endotoxin, and single meals have been shown to raise blood endotoxin, but there are no reports in humans that high fat diet results in metabolic endotoxemia. In addition, there are no established links between gut permeability, metabolic endotoxemia, and skeletal muscle metabolic function in humans. We're recommending that gut function, blood endotoxin, and bone muscle pro-inflammatory signaling and metabolic adaptability be investigated in a healthy human model of acute high fat feeding to investigate the interplay of gut function, blood endotoxin, and metabolic adaptability. We will be running a two-week lead-in period, during which research participants will be introduced to pre-cooked meals that are isocaloric to their normal diet and five days of high saturated fat intake. The transition from isocaloric to habitual diet with a macronutrient profile of 50% fat, 35% carbohydrate, and 15% protein will be included in the high saturated fat feeding period.
Source link: https://clinicaltrials.gov/ct2/show/NCT02328235
After oral glucose intake in humans, the investigators intend to investigate the effects of Kv11. 1 blockade's incretin, insulin secretion, and blood glucose levels. To a 6-hour 75 g oral glucose tolerance test in healthy adults, the investigators of this study hypothesize that Kv11. 1 blockade will raise the metabolic response of serum insulin and GLP-1. The subjects will be wearing a continuous glucose monitor during and after the test and will fill out a glucose questionnaire on the day of the examination. Group A will first be randomized to either group A or B by a qualified unblinded individual from the University of Copenhagen's Department of Biomedical Sciences, 3 days before the test visit, and then, after a 3 weeks washout period, receive a placebo drug prior to test visit 2. The placebo drug will first be available 3 days before test visit 1 and then, after a 3 weeks wash-out period, receive the active drug prior to test visit 2. Immediately prior to and during the same morning as the test visit, receive the test visit 1 and be instructed to orally administer the drug every morning at 6. 00 AM 3 days. Participants will arrive and have a CGM monitor installed 4 days prior to their first and orally administer the medication every morning at the same time as the test visit 2 and on the same morning as the test visit 2. 2nd test visit to the same hospitals as described for Visit 1. Participants must have orally administered the study medications three days before and during the same morning as the test visits were scheduled at the same time. After the last Patient Last Visit, the unblinded individual will do any blindblinding 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 management: The subject and the biological information obtained from the study will be identified by subject number and trial identification number. In cases where laboratory results are shared via non-secure electronic networks, the information will be encrypted during transport. After taking in Kv11. 1 blocker and without Kv11. 1 blocker, an ANOVA will be conducted to see if mean differences exist among study participants. Data analysis plans: To see if mean differences exist among study participants after intake of Kv11. 1 blocker and without Kv11. 1 blocker, an insulin and plasma glucagon, GLP-1, potassium, and GIP concentrations may be found, an ANOVA will be conducted using age and sex as covariate,.
Source link: https://clinicaltrials.gov/ct2/show/NCT03868657
This research is intended to determine whether tadalafil causes subcutaneous adipose tissue to have a "beige" phenotype. Investigators will investigate adipose metabolism using MRI scans and aspiration of subcutaneous adipose from the abdomen. The investigators will perform a cooling protocol to determine the combined effects of tadalafil and on adipose metabolism in comparison to MRI scans at room temperature. The drug's effects on body composition will also be investigated by investigators.
Source link: https://clinicaltrials.gov/ct2/show/NCT04684589
Multiple endocrine neoplasia type 1, familial hypocalcemia, hyperparathyroidism, jaw tumor syndrome, other signs of familial isolated hyperthyroidism, and pseudohypohyroidism are metabolic disorders that are largely inheritable in an autosomal dominant manner. In most FHH kindreds, the CASR gene for the calcium-sensing receptor of the parathyroid cell has been modified; a minority of FHH kindreds have mutations of the GNA11 or AP2S1 gene. HPT-JT is a particular subgroup of familial isolated hyperparathyroidism with components of parathyroid adenoma, parathyroid cancer, jaw tumor, uterus tumor, kidney tumor, and kidney cysts. Parathyroid hormone resistance is one of the determinant G protein's alpha subunits, and one form is linked to mutations in the gene encoding the alpha subunit of the stimulatory G protein.
Source link: https://clinicaltrials.gov/ct2/show/NCT00001345
Non-alcoholic fatty liver disease is the most common hepatic disease in the Western world, and it is a common cause of liver-related morbidity and mortality. The intricate metabolic pathways connecting nutrient intake and hepatic fat accumulation have yet to be fully explained, with excessive caloric intake and specific nutritional factors implicated in its pathogenesis. By using a metabolomics-based dynamic paradigm, we propose a pilot study to examine patients with NAFLD to a standardized 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 monitoring of metabolic rates, and will be given a liquid mixed meal that contains approximately 30% of daily caloric requirements over a period of 15 minutes.
Source link: https://clinicaltrials.gov/ct2/show/NCT02520609
Aim 1 will determine whether blocking enteric neuronal signaling will change: a circulating supply of nutritional substrates and a mystery of hormones that control nutrient metabolism; and b glucose and fatty acid absorption, production, and usage. Until the infusion of glucose and oleic acid into the duodenum, the topical anesthetic benzocaine will be infused into the duodenum. Infusions of a naso-intestinal feeding tube will reduce the confounding effects of gastric emptying on metabolic responses 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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