View clinical trials related to Metabolic Syndrome.
Filter by:The aim of the study is to test whether neutralizing TNF-alpha with infliximab affects insulin resistance and phenotypical manifestations of the metabolic syndrome as fasting plasma insulin, total body fat, plasma lipid profile or vascular endothelial function in obese male subjects.
The increased risk of atherosclerotic morbidity and mortality in patients with obstructive sleep apnea (OSA) has been linked to arterial hypertension, insulin resistance, systemic inflammation, and oxidative stress in previous studies. We aimed to determine the effects of 8-weeks therapy with continuous positive airway pressure (CPAP) on glucose and lipid profile, systemic inflammation, oxidative stress, and the global cardiovascular disease (CVD) risk in patients with severe OSA and metabolic syndrome.
The objective of this intervention study is to examine the effect of n-3 LCPUFA on growth and body composition, intestinal health and microbiotic composition, immune function and risk markers for later diseases in 9-18 months old infants and toddlers.
The aim of the study was to analyse the independent and joint effects of the components of the metabolic syndrome (MetS) on the incidence of diabetes in people with impaired glucose tolerance (IGT) and to assess the effect of acarbose by MetS status. Double-blind placebo controlled trial, 1,368 patients, follow-up time 3.3 years. MetS by ATP III definition with fasting plasma glucose of ≥ 6.1 mmol/l as limit for impaired fasting glucose (IFG).
The purpose of this study is to prospectivly analyze the correlation of triglyceride tolerance and glucose tolerance with cardiovascular morbidity and mortality in patients with stable coronary artery disease within 18 months and to determine, whether measurement of triglyceride tolerance can discriminate patients at risk for cardiovascular events.
The purpose of the study is to determine whether antipsychotic treatment is influence psychiatric patients due to endocrine and metabolic status and a quality of life. The investigators expect, that 30-50% of patients will show pharmacon - gene induced weight gain (> 7% of initial bodyweight) while the rest of patients will maintain unaltered bodyweight.
Lifestyle and genetic factors interact in the development of obesity and the metabolic syndrome. The molecular mechanisms underlying the beneficial dietary modifications are, however, unclear. We aimed to examine the effect of the long-term 30 moderate weight reduction on gene expression in adipose tissue (AT) and to identify genes and gene clusters responsive to treatment and thereby likely contributing to the development of the metabolic syndrome. Thus, randomized controlled and individualized weight reduction and physical exercise intervention was conducted. In the WR group, glucose metabolism improved that was not seen in other groups. Moreover, an inverse correlation between the change in SI and the change in body weight was found (r =-0.44, p=0.026). Down-regulation of gene expression (p<0.01) involving gene ontology groups of extracellular matrix, cell death was seen. Such changes did not occur in the other groups.
We tested the following hypotheses: 1. That a standardized yoga therapy will improve insulin sensitivity (primary outcome), and other features of the metabolic syndrome such as hypertension and dyslipidemia (secondary outcomes), we will perform a 2-hour oral glucose tolerance test, fasting blood tests, and a physical examination before and after randomization of subjects to a 10-week yoga therapy intervention or wait-list control group. 2. That a yoga therapy is feasible in overweight and underactive individuals with the metabolic syndrome, that adherence to a yoga intervention is acceptable, and that yoga therapy is associated with improved quality of life, we will assess the adherence to twice-weekly yoga group sessions (for weeks1-5) and weekly yoga group sessions (for weeks 6-10), frequency of home yoga therapy practice, and self-reported quality of life before and after the intervention in both treatment groups. 3. To elucidate a potential mechanism for the effect of yoga on changes in insulin resistance by evaluating markers of inflammation from adipose tissue (adipocytokines). We hypothesize that these biochemical parameters will show modest improvement with yoga therapy and that changes in these parameters will be associated with improvements in insulin sensitivity.
NAFLD is a spectrum of liver diseases associated with varying degrees of hepatic steatosis, inflammation, and in some cases, fibrosis. NAFLD is a common observation in all demographics, but the prevalence of NAFLD and nonalcoholic steatohepatitis (NASH) is especially high in the morbidly obese population. Leptin is a cytokine that is encoded by the ob gene and primarily secreted by adipose tissue. The production of serum leptin increases with progressive obesity. Because of this observation, there has been significant interest in potential role of leptin in NAFLD. Our hypothesis is that we will find increased hepatic leptin and leptin receptor expression as the degree of hepatic injury worsens in NAFLD.
The purpose of this study is to better understand the link between obesity and diabetes or pre-diabetes.