Active clinical trials for "Metabolic Syndrome"

The main objective of this study is to investigate the role of female sex hormones in relation to insulin resistance in a controlled human experimental model of menopause and to explore whether exercise and/or hormone treatment (HT) can compensate for loss of endogenous sex hormone production by maintaining insulin sensitivity and metabolic activity at a level equivalent to what is seen in premenopausal women. Loss of ovarian function is associated with an increased incidence of metabolic disease including metabolic syndrome, type 2 diabetes and cardiovascular disease. This increased disease incidence seems to be related to changes in body composition including decreased skeletal muscle mass and increased visceral fat mass as well as decreased whole body fat oxidation and energy expenditure. Regular physical activity decreases general mortality among other things by increasing fat free mass and insulin sensitivity and hereby prevents metabolic syndrome and cardiovascular disease - conditions seen with an increased incidence after menopause and could therefore be a possible treatment. In the present study the Investigators will assess the role of sex hormones in a model of menopause where healthy women are undergoing planned bilateral oophorectomy due to risk of hereditary ovary cancer. The use of this model makes it possible to control the time point for loss of ovarian function and hereby investigate the timeframe and possible contributing factors in a strictly controlled model. 48 premenopausal women will be included in the study. The study is conducted in women who have already been offered surgical oophorectomy. The first 2 months the study will be an observational cohort study. Hereafter the patients will be allocated to one of four groups (n=12) in a randomized controlled trial, addressing the effects of 6 months of exercise with or without HT. Type of surgery has been decided before inclusion based on medical indications. The women will be offered HT according to national guidelines, but the choice is up to them. Randomization applies only to the training intervention. Firstly the Investigators aim at investigating the role of endogenous female sex hormones and HT in relation to insulin resistance, whole body fat oxidation and -energy expenditure, changes in visceral fat mass and fat free mass after oophorectomy. Secondly, the Investigators wish to study the molecular mechanisms behind the oophorectomy-induced insulin resistance with a focus on insulin signaling in skeletal muscle and fat tissue. Lastly, the investigators aim to explore whether exercise and/or HT can compensate for loss of endogenous female sex hormone production by maintaining IS and metabolic activity, hereby preventing future incidents of metabolic disease in relation to menopause. All in all, this project will contribute with new knowledge concerning the question of how endogenous female sex hormones affect insulin sensitivity and metabolic functioning and how exercise may be used as a disease preventive modality for middle-aged women.

The link between metabolic disturbances and vitamin D receptor (VDR) and MEGALIN (or LRP2) gene polymorphisms remains unclear, particularly among African-American adults. The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with incident and prevalent metabolic disturbances, including obesity, central obesity and metabolic syndrome (MetS) were evaluated. From 1,024 African-Americans participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS, Baltimore, MD, 2004-2013) study, 539 subjects were selected who had complete genetic data as well as covariates selected for metabolic outcomes at two consecutive examinations (visits 1 and 2) with a mean follow-up time of 4.64±0.93y. Haplotype (HAP) analyses generated polymorphism groups that were linked to incident and prevalent metabolic disturbances.

The study on evaluation the pattern of TD in MetS population may help us to know the magnitude of overlap of these two disease entities and may highlight the importance of thyroid function tests in patients with MetS. This can lead to proper planning and adequate management strategies, resulting in significant reduction in cardiovascular morbidity and mortality due to MetS with TD. Thus, this study aims to evaluate the pattern of TD in patients with MetS and to explore the relationship between TD and components of the MetS.

The purpose of this study is to investigate the prevalence of signs and symptoms of hypogonadism in three groups of testicular cancer survivors.

A pilot randomised controlled trial will be conducted in UiTM Primary Care Clinic, Selayang Campus, Selangor, Malaysia. A total of 232 patients with Metabolic Syndrome (MetS) will be recruited; 116 will be randomised to receive the EMPOWER-SUSTAIN intervention for 6 months and another 116 patients will continue with usual care. The EMPOWER-SUSTAIN intervention is a multifaceted chronic disease management strategies based on the Chronic Care Model (CCM) and persuasive technology theory. It consists of training physicians and patients to use the EMPOWER-SUSTAIN web-based self-management intervention mobile apps, strengthening patient-physician relationship and reinforcing the use of relevant clinical practice guidelines for management and prescribing. The primary outcome is the mean change in patient activation score using the Patient Activation Measure short form Malay version (PAM-13-M) questionnaire. The secondary outcomes include the change in patients' physical activity level, eating behavior, patients' perception on chronic illness care, satisfaction in physician-patient interaction and perceived absolute 10-year cardiovascular disease (CVD) risk.

The project aims to find out the differences between two different types of structured training interventions have on the lipid profile of persons with diagnosed dyslipidemia. Each training intervention will last for 12 weeks. Subjects participating in the project will undergo a series of tests before and after the training intervention which will allow us to make conclusions.

The purpose of this study will be to determine if personalized moderate intensity exercise training combined with high intensity interval training is more effective at improving training responsiveness than moderate intensity exercise training alone? This question will be addressed holistically be creating a composite score to assess training responsiveness. Additionally, individualized biological variability will be calculated in order to quantify training responsiveness using a personalized criterion. It is hypothesized that personalized moderate intensity exercise training combined with high intensity interval training will be more effective at improving comprehensive training responsiveness when compared to moderate intensity exercise training alone?

This study aims at detection of possible associated metabolic syndrome with vitiligo and assessment of possible contribution of the age of onset of vitiligo.

Obesity is an independent risk factor for type 2 diabetes and cardiovascular disease. The increased prevalence of obesity worldwide is a major concern among the scientific and medical communities. Insulin resistance is a common factor associated with obesity, metabolic syndrome, hypertension, and type 2 diabetes. Individuals affected by these conditions often experience endothelial dysfunction as well. Insulin resistance provides a key link between metabolic syndrome risk factors and vascular disease. Development of strategies aimed at preventing vascular dysfunction and future disease caused by metabolic disturbances is needed. Although the relationship between obesity and various diseases is well known, the acute effects of insulin on vascular function in obese individuals have yet to be fully determined. Additionally, the effects of acute exercise on insulin-stimulated endothelial function are unknown. Exercise may be an effective and potent treatment that protects against endothelial dysfunction, insulin resistance, and future cardiometabolic disease commonly present with obesity. However, less attention has been placed on vascular insulin sensitivity. The purpose of this study is to test the hypothesis that a single bout of exercise increases insulin-stimulated blood flow at the macro- and micro-vasculature level in obese individuals with metabolic syndrome to similar levels as healthy obese control. Our laboratory has available non-invasive methods to quantify vascular function and the gold-standard technique for assessing insulin sensitivity (euglycemic-hyperinsulinemic clamp). The investigators will assess vascular function (flow-mediated dilation, post-ischemic flow velocity and contrast-enhanced ultrasound) as well as arterial stiffness (augmentation index and pulse wave velocity) before and at the end of the clamp protocol performed the morning following a bout of exercise and a control (no-exercise) condition in 1) metabolic syndrome and 2) obese adults. If our hypothesis is sustained, it will suggest that a key role of the vasculature exists in regulating insulin following exercise and will provide insight into the link between the vasculature, obesity, metabolic syndrome and cardiovascular disease and may confer decreased risk for cardiometabolic disease.

Pulmonary arterial hypertension (PAH) is characterized by the progressive increase in pulmonary vascular resistance ultimately leading to right ventricular (RV) failure. Its prevalence is estimated at 40-60 persons per million and predominantly affects people between 20 and 60 years of age. Newly available therapies have improved the 3-year survival to >80%. This improvement in prognosis brings new challenges for clinicians: PAH has changed from a rapidly fatal disease to a chronic disorder with persistent exercise limitation and poor quality of life. Many observations suggest that exercise limitation in PAH is not simply due to pulmonary hemodynamic impairment, but that other determinants are involved. Interestingly, even in absence of obesity or diabetes, insulin resistance (IR) and metabolic syndrome (MS) are highly prevalent amongst PAH patients and associated with worse outcomes. Indeed, lipid accumulation in skeletal muscle (a feature of IR) is observed in both human and experimental model of PAH, but its impact on skeletal muscle function and thus exercise intolerance in PAH remains elusive. Over the past years, several pathophysiological pathways activated by MS have been identified, including the downregulation PPARg/PGC1a and the insulin signalling pathways, especially the insulin-receptor substrate 1 (IRS1)-mediated one. The decrease in these axes is associated with lipid accumulation and impaired mitochondrial function. The investigators previously reported in PAH lungs that the downregulation of these pathways contributes to the establishment of the Warburg effect. This metabolic unbalance contributes to pulmonary artery smooth muscle (PASMC) proliferation, and resistance to apoptosis contributing to PA remodelling. The investigators recently documented that PAH skeletal muscles are less perfused and are also characterized by the presence of a Warburg effect. These features were independent of daily life physical activity. Nonetheless, the origin of these abnormalities and their impact on skeletal muscle function have never been studied. The investigators propose to determine whether or not MS seen in PAH patients impairs mitochondrial functions through an IRS1/PPARg/PGC1-dependent mechanism, which will ultimately decrease skeletal muscle function and perfusion, and thus overall exercise capacity.