View clinical trials related to Insulin Resistance.
Filter by:The purpose of this study is to determine whether improvement in fat and muscle metabolism after the treatment with Omacor (fish oils) provides insight into the link between obesity, fat and muscle function leading to metabolic syndrome, which is a risk factor for heart disease and diabetes.
The prevalence of pediatric obesity is increasing at an unprecedented rate. Obese children are at risk for the development of insulin resistance, relative insulin deficiency and type 2 diabetes mellitus. However, the cause of insulin resistance remains an area of scientific interest. The study of type 2 diabetes in children is limited by the lack of a non-invasive method to evaluate insulin resistance. Recent studies have suggested that mitochondrial dysfunction is associated with, and perhaps predictive of insulin resistance in adult relatives of individuals with type 2 diabetes. Mitochondria generate energy in muscle tissue through the production of ATP, and are important in the metabolism of both glucose and fat. This study evaluates a novel, non invasive, safe method for predicting insulin resistance and diabetes in children using a magnetic resonance imaging (MRI) based technique to measure mitochondrial function. We propose to investigate mitochondrial function and glucose metabolism in obese and non-obese children in early, mid and late puberty. Analyses will be conducted to investigate the presence of mitochondrial dysfunction in obese children, to evaluate the contribution of mitochondrial dysfunction to insulin resistance, and to determine the contribution of pubertal status to mitochondrial dysfunction and insulin resistance. The successful completion of this study would provide evidence to support the hypothesis that mitochondrial dysfunction plays a role in insulin resistance and diabetes in children. In addition, it would provide a new technique for the prediction of disease states and perhaps lead to the development of preventative therapeutics for insulin resistance and type 2 diabetes in children. We hypothesize that mitochondrial dysfunction will mirror the progression of insulin resistance and precede and predict abnormal glucose metabolism in a population with pediatric obesity
The goal of the study is to demonstrate whether a switch from insulin therapy to an oral therapy with pioglitazone/glimepiride will lead to a deterioration of glycemic control (increase in HbA1c by more than 0.5 %) within a 6 month observation period.
In parallel with the increasing prevalence of obesity worldwide, type 2 diabetes mellitus (T2DM) has reached epidemic proportions. Despite a multitude of available therapies, only bariatric surgery (e.g., roux-en-Y gastric bypass (GBP)) has proven to be an effective long term treatment modality for morbid obesity. Moreover, the majority of T2DM patients who undergo GBP experience normalization of their blood glucose and are able to discontinue their anti-diabetes medications soon after the procedure. The insulin resistant state commonly seen in non-diabetic obese subjects also improves after GBP. Evidence from recent animal studies suggests that the rapid return to euglycemia seen in T2DM patients after GBP might in part result from excluding the duodenum from the flow of nutrients. With the use of enteral feeding tubes, we hope to better understand the factors in the human gut that may predispose obese individuals to the development of insulin resistance and T2DM.
The purpose og this study is to investigate the effects of growth hormon on insulin signalling pathways and the temporal association between administration of GH and developing of insulin resistance.
Based in a surgery technique studied in a non-obese diabetic mouse model by Rubino and Marescaux(2004), wich reversed diabetes in those animals, we have performed a previous study in human volunteers with type 2 diabetes and overweight (non-obese). The surgery is a duodenal exclusion in wich the stomach volume is kept intact. We observed improvement of glycemic control and hemoglobin A1c, allied to reduction of medicines: insulin was withdrawn or significantly lowered. Further improvement of diabetes could be achieved by intervention in insulin resistance, another factor of diabetes pathophysiology. As that factor is related to visceral fat, we hypothesize that surgical removal of the major omentum, a great component of central adiposity, could beneficial . This study will evaluate the mechanisms of amelioration of type 2 diabetes mellitus after duodenal exclusion surgery plus total omentectomy, by the method of standardized meal stimulus and insulin tolerance test, in human non-obese volunteers with diabetes type 2 and known insulin secretion capacity. The previously studied volunteers submitted to duodenal exclusion without omentectomy will be the control group.
Bariatric surgery leads to remission of type 2 diabetes in morbid obese patients in 80% (Roux-en-Y gastric bypass)to 90% (biliopancreatic diversion and duodenal switch) of cases. The current consensus supports bariatric surgical treatment for diabetic patients with BMI as low as 35kg/m2 but it has questioned that lower body mass patients might benefit of the surgery as well. This study is proposed to describe the effects of Roux-en-Y gastric bypass in mild obese (BMI 30-35) human volunteers on incretins, insulin production and sensitivity and its clinical (diabetic chronic complications) and metabolic impact.
The purpose of this study is to determine if increased intake of low-fat milk products and calcium as part of a calorie restricted diet helps achieve a healthier body weight and body composition and decrease blood glucose levels in people with insulin resistance or type 2 diabetes.
The prevalence of obesity has reached epidemic proportions and is associated with the development of insulin resistance and type 2 diabetes (T2DM). A unifying theme has emerged over the past few years suggesting that lipid oversupply to metabolic organs responsible for glucose regulation leads to insulin resistance. Fitting with this, we and others have shown that increased lipid accumulation within skeletal muscle and/or liver is associated with impaired glucose uptake. However, the underlying mechanisms that mediate changes in muscle lipid metabolism are not yet known. The overall aim of this project is to examine metabolic effects of experimental weight gain in lean and overweight individuals with and without a genetic predisposition to type 2 diabetes. We hypothesise that lean subjects will increase fatty acid oxidation and upregulate mitochondrial oxidative capacity in muscle following overfeeding to protect against body weight gain and insulin resistance, but overweight subjects with a genetic predisposition to T2DM will have a defect in this ability.
Obesity is a strong risk factor for developing type 2 diabetes (T2DM), but the reasons for this are not fully understood. In particular, it is not known why some obese people develop T2DM while other obese individuals do not. This study tests whether differences in fat cells (adipocytes) are to blame. Even in adults, fat cells are constantly being formed to replace old fat cells and to respond to the body's need to store excess energy. The ability to form new fat cells may be diminished in some individuals, leading to larger fat cells. These large fat cells secrete hormones that may increase risk for T2DM. This study tests whether fat cells from obese insulin resistant subjects (who are at risk for developing T2DM) form at a slower rate than those from insulin sensitive subjects (who are at lower risk for developing T2DM). To address this question we will recruit and study two groups of obese subjects, selected to be similar in age, gender and degree of obesity. One group of subjects will be obese and insulin resistant (the OIR group), while the other will be comparably obese, but insulin sensitive (OIS). Subjects will undergo a series of studies to characterize their metabolism including measurement of body fat by DEXA scanning, oral glucose tolerance (a test used to diagnose diabetes) and measurement of insulin sensitivity in response to an infusion of insulin (a research study used to classify patients into the OIR and OIS groups). Small samples of fat (from just under the skin of the belly and the buttocks) will obtained using a needle on two occasions over 12 weeks. During these 12 weeks, subjects will drink a small amount of water that contains a non-radioactive label. This labeled water will allow us to measure the rate of growth of new fat cells in the body. We will also look at the rate of growth of fat cells obtained from these biopsies in the laboratory. The results of this study may tell us more about why certain obese people develop diabetes and why others do not. This might lead to new ways to prevent or treat T2DM.