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 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.
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.
The objectives of this study are to evaluate the safety, tolerance and pharmacokinetics of HE3286 when administered daily for 28 days to obese adult subjects and to assess potential activity of HE3286 to decrease insulin resistance. An open-label cohort of 6 patients with type II diabetes mellitus will be treated at 10 mg (5 mg BID).
Physical inactivity induces vascular dysfunction and glucose intolerance during five days of bed rest. This study will investigate the effects of salsalate on these responses. Subjects will be randomized to treatment with salsalate or placebo for four days prior to initiation of bed rest. Vascular function in the brachial artery will be determined by ultrasound prior to treatment and before and after the 5-day bed rest protocol. We hypothesize that treatment with salsalate will be associated with protection again the development of glucose intolerance and vascular dysfunction in this setting.