Active clinical trials for "Metabolic Diseases"

This is a prospective, non-randomized, non-blinded observational study. The overarching goal is to discover new disease-associated genes in children, while establishing a specific focus on disorders where molecular characterization is most likely to lead to novel therapies. This study will merge detailed phenotypic characterization of patients presenting to the Pediatric Genetics and Metabolism Division in the Department of Pediatrics/Children's Medical Center at Dallas and collaborating clinics with Next-Generation sequencing techniques to identify disease-producing mutations. The primary objective of the study is to identify novel pathogenic mutations in children with rare Mendelian disorders. A secondary objective of the study is to establish normative ranges of a large number of metabolites from healthy newborns and older children.

The project will use carbon-13 magnetic resonance spectroscopy to assess whether high glycogen levels in skeletal muscle of patients with Glycogen Storage Diseases is a prelude for muscle damage. Patients with Glycogen Storage Diseases will be examined using carbon-13 MR-spectroscopy to quantify the glycogen levels in lumbar, thigh and calf-muscles. The pattern of glycogen concentration will be compared to the pattern of muscle atrophy found in the literature.

This study is a prospective, randomized, open-label, multi-center trial. The primary objective of the study is to assess whether XZK 1200mg/d, compared to atorvastatin 20mg/d, has a favorable impact on HbA1c levels at 24 weeks of treatment in dyslipidemia patients with prediabetes

From a scientific point of view and for publication purposes, it therefore seems important to study the metabolism of iron and in particular to define its conditions of absorption, metabolism, elimination and storage in the body at course of advanced renal failure. The study will follow the evolution of hormones regulating iron metabolism and put into perspective their links with phosphocalcic and hepatic metabolisms as well as inflammation in hemodialysis patients. The main objective of this program is to study the evolution of hepcidin and erythroferrone levels in hemodialysis patients. These two biomarkers regulating iron metabolism are not performed routinely in dialysis centers and are not listed in the nomenclature.

This is a study of biomarkers obtained from prospectively collected subject samples and their correlation with cardiovascular and metabolic diseases. The purpose of this initiative is to develop an enduring tool to allow for collaborative research between clinicians at Cleveland Clinic Main Campus and basic scientists at the Lerner Research Institute. This collaboration will allow resources to be available to clinical and basic researchers alike. This tool will enable research of vascular disease in the Vascular Lab and will leverage this valuable asset to the fullest extent to allow for interdepartmental collaboration.

This study aims to understand the state of onset of NLSD(neutral lipid storage disease) / TGCV(triglyceride deposit cardiovasculopathy) worldwide, background information of affected patients, and natural history of the disease, as well as exploring the prognostic factors and assessing the efficacy of disease-specific treatment.

When muscles are not contracting, the local energy demand by muscle and use of specific fuels used to produce energy by oxidative metabolism are minimal. The time people spend sitting inactive (sedentary time) typically comprises more than half of the day. This sedentary behavior is associated with elevated risk of diabetes, cardiovascular diseases, some cancers, and multiple conditions leading to poor aging. From a progressive series of experiments, the driving goal is to develop a physiological method for sustaining contractile activity via oxidative metabolism over more time than is possible by traditional exercise (hours, not minutes per day). Developing a physiological method suitable of prolonged muscular activity for ordinary people (who are often unfit) requires gaining fundamental insights about muscle biology and biomechanics. This also entails a careful appreciation of the ability to isolate specific muscles in the leg during controlled movements, such as the soleus muscle during isolated plantarflexion. This includes quantifying specific biological processes that are directly responsive to elevated skeletal muscle recruitment. The investigators will focus on movement that is safe and practical for ordinary people to do given their high amount of daily sitting time. This includes developing methods to optimally raise muscle contractile activity, in a way that is not limited by fatigue, and is feasible throughout as many minutes of the day as possible safely. This also requires development of methodologies to quantify specific muscular activity, rather than generalized body movement. There is a need to learn how much people can increase muscle metabolism by physical activity that is perceived to them as being light effort. It is important to learn if this impacts systemic metabolic processes under experimental conditions over a short term time span in order to avoid confounding influences of changes in body weight or other factors.

Type 2 diabetes is a chronic condition that affects the ability of the body to regulate glucose (sugar). When glucose levels are low, the liver can make glucose to increase levels in the body. This important process is called endogenous glucose production (EGP). Previous studies suggest that the central nervous system (CNS), including the brain, helps to coordinate this process by communicating with the liver through potassium channels. Control of EGP can be impaired in people with type 2 diabetes, which may contribute to the high levels of glucose seen in these individuals. The purpose of this study is to understand how activating these potassium channels in the control centers of the brain with a medication called diazoxide might inhibit the amount of glucose made by the liver. This is particularly important for people with diabetes who have very high production of glucose, which in turn causes hyperglycemia (high levels of sugar in the blood) that leads to diabetes complications.

The goal of this clinical trial is to explore the role of wheat and corn germ blended oils in regulating oxidative stress and immunomodulation in dyslipidaemic populations, to explore their effects on intestinal flora, antioxidant and immunomodulation. The main questions it aims to answer are: How does phytosterol-rich wheat corn germ blended oil affect oxidative stress and immune function in dyslipidaemic people compared to peanut oil? How does phytosterol-rich wheat corn germ blended oil affect serum metabolites, serum fatty acid profile, and intestinal flora in dyslipidaemic populations compared to peanut oil? What are the specific mechanisms involved? Participants will be randomly assigned to the intervention and control groups, the packaging of germ oil and peanut oil will have a uniform appearance, and participants will be instructed to replace their household cooking oils with the distributed cooking oil for three months, in addition to replacing all the canteens in the staff units with the trial oil for more than three months. Participants did not know who was the control oil, germ oil or peanut oil, and both were randomly distributed to different groups of participants by the third-party supervisors. Researchers will compare peanut oil to see if phytosterol-rich germ oil can improve oxidative stress and immune function in dyslipidaemic populations, in addition to exploring possible underlying mechanisms of improvement using multi-omics techniques.

Dietary interventions have been consistently proposed as a part of a comprehensive strategy to lower the incidence and severity of atherosclerosis and cardiovascular diseases (CVD). Excessive consumption of fats enriched in saturated fatty acids (SFA) is associated with an increased risk of atherosclerosis and other CVD. By contrast, replacement of SFA with monounsaturated fatty acids (MUFA) and omega-3 long-chain polyunsaturated fatty acids (ω-3 PUFA) has been reported to be inversely associated with risk of atherosclerosis. This is partly due to the ability of MUFA (and PUFA) in modulating low-density lipoprotein (LDL) and triglyceride-rich lipoprotein (TRL) lipid composition and oxidation status, and thereby the functionality of such lipoproteins. While most of the nutritional studies have focused on elucidating the mechanisms by which dietary fats affect LDL and TRL, little or nothing is known about the regulatory effect of MUFA and PUFA on structure and functional remodelling of high-density lipoproteins (HDL). There is clear evidence of an inverse association between plasma levels of HDL and the formation of atherosclerotic plaques. However, recent studies have suggested that HDL may not be as beneficial as thought at least in patients with established cardiometabolic disorders. In those patients, the HDL behaves as pro-inflammatory lipoproteins. Until now, few studies have addressed this "dark side" of HDL and has never been evaluated the role of dietary fatty acids on HDL plasticity (i.e. phenotype and functionality). A better understanding of this duality between anti-inflammatory and pro-inflammatory HDL would be relevant to prevent HDL-related atherogenic dyslipidemias and to provide personalized dietary advices for a successful management of atherogenic lipid profiles. This step of proof-of-principle will determine the instrumental role of major fatty acids present on a diet (SFA, MUFA and MUFA plus ω-3 PUFA) in promoting or reversing the phenotype of pro-inflammatory HDL. We expect to offer a novel insight on HDL and its relationship with dietary fatty acids through the following objectives: 1) To analyse acute changes in the lipidome, proteome and functional properties of HDL in humans (healthy volunteers and patients with metabolic syndrome) upon a challenge of a meal rich in SFA, MUFA or MUFA plus ω-3 PUFA; and 2) To analyse the influence of diets rich in SFA, MUFA and MUFA plus ω-3 PUFA on HDL plasticity in a preclinical animal model of diet-induced metabolic syndrome and that develops atherosclerosis.