View clinical trials related to Prediabetic State.
Filter by:Oxidative stress is produced by imbalance between reactive oxygen species and antioxidant systems. This state is frequently associated with chronic diseases like obesity, insulin resistance, metabolic syndrome and hepatic steatosis. In the liver, the oxidative stress may trigger the progression of fatty liver disease, from triglyceride accumulation to inflammation, cirrhosis and hepatocellular carcinoma. Thus, the attenuation of oxidative stress, could be an important therapeutic target to lessen the severity of the disease. Until now, there is not a medical treatment to cure non-alcoholic fatty liver disease, but therapies aimed at reducing oxidative stress have been proposed. Metadoxine, an ionic complex of pyridoxine-pyrrolidone molecule, acts as a synthetic antioxidant, forming traps that can reduce free radicals; likewise, metadoxine has a proven capacity to reduce fat liver in alcoholic hepatitis. Finally, in fact that alcoholic and non-alcoholic liver diseases share molecular mechanisms in the generation of oxidative stress, the investigators propose metadoxine as a posssible modifier of the oxidative stress in non-alcoholic liver disease, prediabetic patients.
Background: Type 2 diabetes mellitus is a main risk factor for cardiovascular disease and heart failure, in part due to diabetic cardiomyopathy. However, the association between intracellular lipid accumulation and (myocardial) functional impairment is likely more complex than originally imagined. Recent studies suggest that not fat per se, but the content of saturated or unsaturated fatty acids might predict the development of cardiac steatosis and myocardial dysfunction. In addition skeletal muscle and hepatic glycogen metabolism is impaired in patients with diabetes mellitus. Data from animal experiments suggest a relevant role of myocardial glycogen stores in ischemic preconditioning. Due to methodological limitations so far data on myocardial glycogen stores and myocardial lipid composition in humans are missing. Hypothesis: In addition to total ectopic lipid deposition in the myocardium, myocardial lipid composition, i.e. the relative abundance of saturated and unsaturated fatty acids, and impaired myocardial glycogen metabolism may play an important role in the development cardiac lipotoxicity leading to diabetic cardiomyopathy. Pancreatic endocrine function and myocardial morphology and function is altered in patients with heterozygote inactivating mutations of the CaSR-gene / FHH. Aims: - Metabolic virtual biopsy of the myocardium for identification of specific patterns of intracellular lipid composition and myocardial glycogen metabolism as possible critical determinants of metabolic cardiomyopathy - Characterization of the metabolic interplay between the myocardium, skeletal muscle, liver and adipose tissues in different stages of development of type 2 diabetes compared to patients with calcium sensing receptor mutation Methods: - 1H/13C and 31P magnetic resonance spectroscopy and imaging for measurements of myocardial, skeletal and liver lipid and glycogen content, abdominal adipose tissue distribution and composition, ATP synthesis and myocardial functional parameters - Mixed meal tolerance tests to trace the postprandial partitioning of substrates between insulin sensitive tissues (myocardium, skeletal muscle, liver, adipose tissue). - Hyperinsulinemic-hyperglycemic glucose clamp (HHC) with enrichment of the infused glucose with the stable isotope [1-13C]glucose to trace the incorporation of circulating glucose into myocardial glycogen in healthy insulin sensitive volunteers, prediabetic insulin resistant volunteers with impaired glucose tolerance, healthy subjects, patients suffering from type 2 diabetes mellitus, patients suffering from type 1 diabetes and patients with heterozygote mutation in calcium sensing receptor.
The undercarboxylated fractions of the two vitamin K-dependent proteins osteocalcin and matrix Gla protein have been shown to play key roles in type 2 diabetes and cardiovascular disease (at least in mouse models). Clinical trials are needed to isolate the effects of vitamin K manipulation on carboxylation of these two proteins (osteocalcin and matrix GLA protein) and their subsequent effects on markers of diabetes and cardiovascular disease risk. The purpose of this pilot randomized, double-blind, placebo-controlled trial in children is to estimate the effective dose of vitamin K2 (menaquinone-7) supplementation (to improve carboxylation of both osteocalcin and matrix Gla protein), and whether it can have an effect on markers associated with diabetes and cardiovascular disease risk.
The purpose of the study is to examine the effect of Saxagliptin in the newly diagnosed people with pre-diabetes and obesity besides lifestyle intervention ,there to evaluate DPP 4 inhibitors of reversing pre-diabetes curative effect to normal blood sugar, and observe its influences on the targets of obesity related metabolic abnormalities, to explore new ways for intervention on populations with pre-diabetes and obesity .
Evaluate the effects of rosuvastatin (maybe the highest diabetogenic) and pravastatin (seems to be protective) on the glucose homeostasis and other biomarkers in subjects with impaired fasting glucose.
The purpose of this study is to determine if a 6-month community-based prediabetes lifestyle and behaviour change intervention (called, PREPARE) for middle and older adults with prediabetes will result in positive lifestyle behaviour change.
Many adipokines are thought that related with metabolic disturbance such as glucose intolerance, dyslipidemia, and insulin resistance. It is reported that regular physical training could prevent the progression of diabetes from prediabetes and improve the insulin resistance. After physical training, many adipokine levels were changed due to improving insulin resistance. In this study, we will examine the various adipokine levels such as adiponectin, RBP-4, and adrenomedullin after exercise training through exercise prescription in IFG and IGT patients.
We, the investigators at National Taiwan University Hospital, want to compare patients' islet cell function, insulin sensitivity and risk of chronic complications with normal subjects. Moreover, we want to examine whether they are at a higher risk of having metabolic syndrome and to answer whether we should screen the phenotypes of metabolic syndrome in impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) patients. Then, we want to examine the association between insulin sensitivity and islet functions.