View clinical trials related to Metabolic Syndrome X.
Filter by:The purpose of this study is to determine whether obese people do not respond to hepatitis C treatment as well as lean people. This research studies whether obese people will show higher sustained virologic response rate if they lose weight by Orlistat use and dietary and lifestyle modification.
The purpose of this study is to characterise beta cell function in subjects who despite taking part in a diabetes prevention program (life style intervention with diet and exercise) exhibit impaired glucose tolerance and beta cell dysfunction.
The purpose of this study is to determine if a low fructose intake could have an impact on weight loss, uric acid levels and the components of the metabolic syndrome (glucose, cholesterol, triglycerides, insulin resistance, high blood pressure).
The aim of this study is to assess the frequency of metabolic syndrome in Down syndrome patients because the prevalence of diabetes mellitus and obesity is higher in individuals with Down syndrome than in the general population.
The overall goal of this study is to determine whether variations in the perilipin, and several other, genes would be a useful tool for physicians who are caring for morbidly obese patients to guide therapy. The main hypotheses to be tested is that sequence variations (polymorphisms) in the perilipin gene and several other obesity-related genes are associated with resistance to weight loss for obese individuals on energy restricted diets, potentially playing a role in the development of obesity related complications.
The purpose of this study was to determine whether patients with schizophrenia, schizoaffective disorder, or bipolar I disorder who also have metabolic syndrome have a larger decrease in fasting non-high density lipoprotein (non-HDL) cholesterol levels with aripiprazole than with their current atypical antipsychotic treatment (olanzapine, risperidone, or quetiapine).
Heart disease is the most common cause of death in the United States and it is commonly found in people with diabetes and high cholesterol. Inflammation is one mechanism by which diabetes and elevated cholesterol damage blood vessels. Inflammation can be increased by oxidative stress. This study will see if Alpha Lipoic acid, a potent antioxidant and over the counter product, reduces blood levels of markers of oxidative stress and inflammation when compared with placebo. Placebo is a substance that looks like the real product, but contains no active product.
Obese HIV-positive women with Metabolic Syndrome (HIV-MS) and obese HIV-negative women with Metabolic Syndrome will be studied before and after achieving moderate (6%-8%) diet-induced weight loss. The investigators hypothesize that health markers will improve in both groups but that the improvement will be blunted in the women with HIV-MS.
Glucagon-like peptide 1 (GLP-1) is an intestinal peptide hormone secreted in a nutrient-dependent manner that stimulates the pancreatic beta cells to secrete more insulin in response to the same amount of blood glucose. In patients with Type 2 diabetes, GLP-1 secretion is lower than normal, thus suggesting that the hormone may contribute to the pathogenesis of the disease. Whether infusion of GLP-1 affects endothelial function and glucose uptake in humans has never been investigated. In the current proposal, the investigators hypothesize that GLP-1 administration might ameliorate endothelial dysfunction in patients with metabolic syndrome. To test this hypothesis, the investigators will evaluate the acute effects of GLP-1 in the forearm circulation of patients with metabolic syndrome during local hyperinsulinemia by use of the forearm perfusion technique.
Thrombin is the most potent activator of platelets, and platelet activation is a hallmark of thrombosis. Coronary artery disease (CAD) is the major cause of mortality and morbidity in the United States and other industrialized countries, and thrombotic sequelae are the key cause of death in diabetes. The accumulation of thrombin at sites of vascular injury provides one of the major mechanisms of recruiting platelets into a hemostatic plug. Thrombin works by activation of the G protein-coupled protease activated receptors PAR1 and PAR4 on human platelets to initiate signaling cascades leading to increases in [Ca]i, secretion of autocrine activators, trafficking of adhesion molecules to the plasma membrane, and shape change, which all promote platelet aggregation. The thrombin receptors work in a progressive manner, with PAR1 activated at low thrombin concentrations, and PAR4 recruited at higher thrombin concentrations. As direct thrombin inhibitors become widely used in clinical practice, it is important to assess their effects on vascular function. Our hypothesis is that PAR1 and PAR4 do not signal through the same G protein pathways, and that PAR4 is not a strong platelet agonist. To investigate this hypothesis, the investigators will study the G protein pathways downstream of PAR4, and assess ex-vivo platelet responsiveness to thrombin, PAR1, and PAR4 agonist peptides, both in normal human subjects, and along the stages of pathology, from patients with stable angina as well as unstable angina who are undergoing angioplasty. Similarly, the investigators will examine platelet function in patients with metabolic syndrome as well as diabetes, along the continuum from insulin resistance to full-blown disease. These studies will provide deeper insight into the G protein pathways used by PARs. They will elucidate the contribution of PAR receptors to normal platelet function as well as the abnormal platelet activation in thrombotic states. The long term goal is to understand the implications for PAR receptors as therapeutic targets for anti-platelet therapies that may carry less bleeding risk.