View clinical trials related to Metabolic Syndrome.
Filter by: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.
Almost all of antipsychotics can induce metabolic syndrome,Genetic factors play a key role in the development of metabolic syndrome,TCF7L2 and SLC30A8 are strongestly correlated with metabolic syndrome.Moreover,Antipsychotics have an effect on the expression of TCF7L2 and SLC30A8 genes.It indicates the variations of TCF7L2 and SLC30A8 play an important part in the development of antipsychotics-induced metabolic syndrome.
Aim : Investigated the effects of Korean red ginseng supplementation on metabolic parameters such as cholesterol, blood pressure and glucose. Randomized Control Trial.
There is some evidence to suggest that obesity is a risk factor for the development of cognitive dysfunction, although this is not a universal finding. This discordance might be ascribed to the existence of a 'healthy obese phenotype'- that is, obesity in the absence of metabolic risk factors. We examined whether the association of obesity with cognitive dysfunction is dependent on the individual's metabolic health. 60 obese patients' undergoping liver fibroscan and blood tests will be enrolled. Obesity was defined as body mass index ≥ 30 kg/m2. Based on blood pressure, HDL-cholesterol, triglycerides, glycated haemoglobin, and C-reactive protein, participants were classified as 'metabolically healthy' (0 or 1 metabolic abnormality) or 'unhealthy' (≥ 2 metabolic abnormalities). Cognitive dysfunction will be assessed by moca and minimental score. Results: Cognitive dysfunction prevalence is expected in 30% , but 50% of this group was categorized as metabolically healthy. Relative to non-obese healthy participants, after adjustment for baseline covariates, the metabolically unhealthy obese participants had elevated risk of cognitive dysfunction although the metabolically healthy obese did not. The association between obesity and risk of cognitive dysfunction appears to be partly dependent on metabolic health, although further work is required to confirm these findings. In obesity there is an increase in oxidative stress due to metabolic syndrome . Thus obese patients suffer from higher incidences of cardiovascular complications such as atherosclerosis as compare to non- obese population. Haptoglobin (Hp) is a plasma protein which binds free hemoglobin and prevents it from heme- iron mediated oxidation. There are three different types of Hp which differ in their antioxidant ability. Several clinical studies have shown that Hp 2-2 genotype is associated with higher incidence of cardiovascular diseases.
Elevated subconscious nervous system activity is a characteristic of the obese state and contributes importantly to the risk of heart disease and diabetes. This project will compare sympathetic nervous system activity and function in a group of obese persons with differing levels of sugar tolerance (normal, impaired and type 2 diabetic). Inter-relationships with insulin action, blood pressure, heart and kidney function will be determined before and after a 4-month weight loss and 3-month weight loss maintenance program. It is hypothesized that the transition from normal sugar tolerance to impaired sugar tolerance to type 2 diabetes will be accompanied by escalating sympathetic nervous system dysfunction. Furthermore, that weight loss will favorably improve sympathetic function, with greatest benefits occurring in those subjects who are insulin resistant with high blood insulin concentration.
Aim 1 is to study prevalence and 1 year incidence of metabolic syndrome in major depressive disorder and factors correlation. Aim 2 is to study prevalence and 1 year incidence of thyroid dysfunction in major depressive disorder and factors correlation.
The aim of this study is to examine the prevalence of the Metabolic syndrome(MetS) in Korean patients with schizophrenia. Primary objective: • To investigate the prevalence of the MetS in Korean patients with schizophrenia Secondary objectives: • To compare the prevalence of the MetS among 3 groups according to antipsychotics: typical antipsychotic monotherapy group, atypical antipsychotic monotherapy group, 2 or more antipsychotics group (polypharmacy)
Current obesity prevention emphasizes caloric restriction and avoidance of high fat foods. The result is an approach that replaces dietary fat with carbohydrates. There has, however, since been an obesity epidemic with an increased prevalence of metabolic syndrome (MetS) and type II diabetes. Negative results from trials of low fat diets for weight loss, prevention of heart disease and malignancies are consistent with the inadequacy of low fat/high carbohydrate approach. One of the findings of trials comparing low fat, calorie reduced diets to ad lib carbohydrate restricted diets is that subjects randomized to a low carbohydrate intake lose more weight despite equivalent intake. This equates to a 200 kcal/day greater weight loss on a carbohydrate restricted diet. Some investigators have speculated the metabolic advantage of carbohydrate restriction is due to increased energetic costs of gluconeogenesis. Alternatively, carbohydrate restriction is associated with increases in spontaneous physical activity. This protocol has three aims. First, adherence to a carbohydrate restricted diet in subjects with metabolic syndrome will cause an increase in spontaneous physical activity, independent of weight changes. Second, cardiometabolic risk factors (ApoB, TG, HDL, blood pressure, CRP) will show greater improvement on a carbohydrate restricted diet compared to a low-fat, high carbohydrate diet. Finally the investigators will interview a sub-sample of participants to better understand quality of life issues with respect to the dietary assignment or lifestyle intervention. The investigators will recruit 72 participants with MetS, from the Metabolic Syndrome Program at St. Paul's Hospital, Vancouver. Individuals will be randomized to either a low-carbohydrate diet or a calorie restricted, low fat diet and followed for 6 months. The investigators will measure body composition with bioelectrical impedance at baseline, 3 and 6 months. The investigators will also examine cardiometabolic changes due to the standard lifestyle intervention compared to the carbohydrate restricted treatment. The investigators will examine blood pressure, triglycerides, LDL-chol, HDL-chol, C-reactive protein, apolipoprotein B, glucose, insulin, hemoglobin A1c and leptin at baseline, 3 and 6 months. The investigators will use accelerometers to assess changes in physical activity. The investigators will use three-way repeated-measures ANOVA, with changes in body weight and insulin levels as covariates in the model with time as the repeated factor for statistical analyses.
Fructose intake from added sugars has increased dramatically over the last century and has recently been implicated as potential contributor to metabolic syndrome, obesity, hypertension, inflammation and kidney disease. Fructose differs from the other sugars because, uric acid is generated during its metabolism. Serum uric acid levels have been found to correlate with the intake of fructose and added sugars. In turn, an elevated serum uric acid has also been shown to be associated with increased risk for cardiovascular and metabolic diseases. On the other hand complexity of fructose metabolism in each individuals results of the various magnitude of hyperuricemia induced by fructose intake. The magnitude of uric acid production in each patient may reflect individual predisposition to endogenous urate production in a face of relatively normal fasting uric acid concentration. Therefore the oral fructose tolerance test might reveal an occult purine disturbances which plays casual role in either metabolic disturbances or organ damage. The aim of this study is to see whether is a relationship between fructose induced hyperuricemia and metabolic disturbances , inflammatory state and organ damage in obese and various stages CKD patients.
The metabolic syndrome is a collection of related risk factors that predispose to the development of type 2 diabetes Mellitus and cardiovascular disease. The investigators will examine the hypothesis that the metabolic and genomic characteristics of patients with metabolic syndrome and/or diabetes that are at risk for developing complications differ from each other and can be detected using specific biomarkers in blood or in the exhaled breath. Early detection of these individuals will enable personalized treatment to prevent and treat diabetes and its complications