Active clinical trials for "Metabolic Syndrome"

Intestinal metaplasia is generally considered a precancerous lesion. Although it is associated with a very small increase of gastric cancer risk, European Endoscopic Society and other European academic companies highlighted the increased risk of cancer in patients with gastric atrophy and IM and the need for staging in cases with high-grade dysplasia. The production of ROS in the gastrointestinal tract (GI) and their role in the pathophysiology and pathogenesis of gastrointestinal diseases have not been studied sufficiently. In the plasma of patients, in the context of the sequence gastro oesophageal reflux-oesophagitis-metaplasia-dysplasia-adenocarcinoma, have been found simultaneous formation of DNA adducts and increased myeloperoxidase concentration, which are associated with oxidative stress, decreased antioxidant capacity (decreased glutathione concentration).These findings support the role of oxidative stress in the pathogenesis and malignant transformation. Metabolic Syndrome (MS) has been recognized as a pro-inflammatory, pro-coagulant state associated with increased levels of C reactive protein (CRP), interleukin (IL) 6 and plasminogen activator inhibitor (PAI) 1. It has been reported that the inflammatory and the pro thrombotic markers, which are associated with increased risk for cardiovascular disease and DM2, represent only a part of the relationship between IM and cardiovascular mortality. Several factors influence the pathogenesis of MS, as the pro-oxidant condition of such patients may increase the risk for developing symptoms and related chronic diseases such as DM2. Although the exact contribution of oxidative stress on every pathologic condition included in MS is difficult to determine definitively, it is certain that oxidative stress is particularly high in the MS. Regarding the relationship between MS and GI diseases, studies have reported that patients with MS are almost twice at risk for developing Barrett's esophagus.The relationship between MS, gastro-esophageal reflux disease (GERD), and the development of IM also requires well designed prospective studies. It seems however, to be a correlation between obesity and GERD, as well as between obesity and gastric adenocarcinoma

Attainment of peak healthy lung function during the 18-26 yr window is a strong determinant of the rate of lung function decline during the later years of life. The attainment of a healthy peak lung function is mediated by pre and peri natal exposures ( in utero environment and nutrition) and exposure to environmental toxicants and nutrition during childhood and early adulthood. Towards this Indian birth cohorts, having collected comprehensive data on maternal nutrition and anthropometry can provide invaluable insight into the factors affecting lung function growth and their effect sizes in the Indian population. Therefore, in this observational study, the Investigator will be collecting data on lung function, current nutritional and environmental exposures and linking it to pre and peri natal data of the same participants in order to understand lung function growth and the reasons for an early decline in the Indian population, using a life course approach.

Since uncontrolled observational studies first linked fructose to the epidemic of obesity almost a decade ago, it has become a focus of intense concern regarding its role in the obesity epidemic. Despite the uncertainties in the evidence,the recommendations of international health organizations have cautioned against moderate to high intakes fructose-containing sugars, especially those from sugar sweetened beverages (SSBs). To improve the evidence on which nutrition recommendations are based, the investigators propose to study of the effect of fructose-containing sugar sweetened beverages (SSBs)on body weight, by undertaking a systematic synthesis of the data taken from all available clinical studies in humans. This technique has the strength of allowing all of the available data to be pooled together and differences to be explored in groups of different study participants (healthy humans of different sex, weight, and age and in those with diseases which predispose to disturbances in metabolism, such as diabetes) with dietary fructose in different forms, doses, and with differing durations of exposure. The findings generated by this proposed knowledge synthesis will help improve the health of consumers through informing recommendations for the general public, as well as those at risk of diabetes and cardiovascular disease.

Vegetarian diets have been associated with a reduced risk of preventable diseases such as type 2 diabetes and cardiovascular disease. These effects may be mediated through direct or indirect pathways. Although the high intakes of nuts, legumes, dietary fibre, whole grains, and unsaturated plant oils have each individually been associated with lower risk of type 2 diabetes and cardiovascular disease, so too has the displacement of red meats, processed meats, and saturated animal fats. One of the most important considerations in moving from animal-based diets to more plant-based diets is the replacement of animal proteins (e.g. meat, fish, dairy, eggs) with vegetable proteins (e.g. legumes, nuts, and seeds). It is unclear whether this particular replacement alone results in advantages for metabolic and cardiovascular health. To improve evidence-based guidance for dietary guidelines and health claims development, we propose to conduct a series of systematic reviews and meta-analyses of the effect of plant-based protein in exchange for animal protein on blood lipids, glycemic control, blood pressure, body weight, uric acid, markers of non-alcoholic fatty liver disease (NAFLD), and kidney function and injury. The systematic review process allows the combining of the results from many small studies in order to arrive at a pooled estimate, similar to a weighted average, of the true effect. The investigators will be able to explore whether the effects of replacing animal-based protein for plant-based protein hold true across different sexes, age groups, and background disease states and whether the effect depends on the protein source, dose, or background diet. The findings of this proposed knowledge synthesis will help improve the health of Canadians through informing recommendations for the general public, as well as those at risk of heart disease and diabetes.

Jangzhuo Qinggan prescription and irbesartan in the treatment of essential hypertension(Hepatogastric Damp-heat), randomized, parallel-controlled, multi-center clinical study.

Primary aldosteronism (PA) is occasionally associated with impaired glucose tolerance. Glucose intolerance, in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues. Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion. It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA. The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. The conclusion with respect to the possible causal relationship between diabetes mellitus (DM) and PA, however, can be obtained after the evaluation of the effect of surgical /pharmacological treatment of PA.

In the UK, 25% of the adults are affected by metabolic syndrome (NHS, 2016). Metabolic syndrome is a cluster of different conditions including: hyperglycaemia, insulin resistance hypertriglyceridemia, dyslipidaemia and hypertension. Such individuals also have increased risk of developing type 2 diabetes and cardiovascular disease. The factors contributing to the development of metabolic syndrome are potentially numerous and understudied in humans, with much of what we think we know coming from animal research. Recent animal studies have pointed towards gut health playing a role in metabolic health. More specifically it has been suggested that changes in the composition of the gut microbiota may drive insulin resistance and type 2 diabetes through a mechanism that is linked to increased gut permeability and the development of metabolic endotoxemia and inflammation. Yet, this link has not been confirmed in humans. This research will look at the relationship between diet, physical activity, sleeping patterns, obesity status and age etc. and measures of gut bacterial composition, gut barrier function and metabolic health. Findings will provide us with new insights on the effect of different physiological and behavioural/ lifestyle variables on gut health and metabolic function.

Metabolic syndrome (MS) is a public health problem characterized by central obesity, increased blood pressure and triglyceride levels, decreased blood HDL levels and the presence of insulin resistance (1).Kinesiophobia is a fear of irrational movement that develops because of its belief in susceptibility to injury and is associated with low levels of physical activity. Considering that exercise improves metabolic processes in people with MS, we aimed to evaluate the presence of kinesophobia in patients with MS. Patients aged 45-65 years diagnosed with metabolic syndrome and healthy controls will be included in the study. Patients with rheumatic and neurological diseases,history of trauma, gonarthrosis, lumbar disc hernia, previous fractures, fibromyalgia and those who have experienced pain for the last week will be excluded. The participants will be filled in the Short Form-36 (SF-36), the Hospital Anxiety and Depression Scale, and the Tampa Kinesiophobia Scale. 48 patients with MS and 48 healthy participants will be included in the study.

This study aims to evaluate, at long-term, the occurrence of liver disease and cardio-vascular risk, in a sample of patients diagnosed with first episode of non-affective psychosis.

This study will be undertaken to evaluate the association of serum uric acid (SUA) level with metabolic risk factors in patients with type 2 diabetes and their relation to eGFR status