View clinical trials related to Insulin Resistance.
Filter by:Thiazolidinedione derivates (TZD's) are Peroxisome-Proliferator-Activated-Receptor-γ agonists (PPARγ-agonists) and enhance insulin sensitivity. One of the side effects, however, is the fact that subjects treated with these drugs seem to be more prone to fluid retention. The precise mechanism of rosiglitazone-related fluid retention is unknown, but it is clear that either primary or secondary renal sodium retention is part of the mechanism. Furthermore in observational studies, TZD-related oedema seems to be resistant to loop diuretic therapy. The recent finding that rosiglitazone induces upregulation of the epithelial sodium channel (ENaC) in the kidney could be the explanation for TZD-related fluid retention and the observed resistance to loop diuretics. In the present human in-vivo study the following hypothesis will be tested: Rosiglitazone treatment stimulates the activity of ENaC in the distal nephron, which enhances the natriuretic effect of amiloride and decreases the natriuretic effect of furosemide in parallel.
Determine if men with erectile dysfunction (ED) are more likely to have insulin resistance compared to healthy controls.
The investigators hypothesise that a common A277G polymorphism of the liver fatty acid binding protein (L-FABP) gene, which leads to an amino acid exchange, may be associated with alterations of lipid-induced hepatic insulin resistance. In the present study the investigators will investigate potential differences in lipid-induced hepatic insulin resistance, and in the relation between glycogenolysis and gluconeogenesis, in healthy subjects with the A277G polymorphism vs. subjects carrying the wildtype.
This study aims to understand the biological processes that link obesity to diseases including insulin resistance and diabetes. Our approach involves studying the health of patient undergoing weight loss either via weight reduction surgery or by medically supervised liquid formula diets. Patients must be enrolled in a weight treatment program at Emory Bariatrics, Emory University, Atlanta GA, to be eligible for this study. This study does not cover the cost of treatment at Emory Bariatrics. The hypothesis is that decreases in adipose-tissue derived factors during weight loss will be related to improvement in insulin function.
This study will investigate the separate and combined effects of aerobic and resistance training on cardiovascular risk factors in overweight men and women with mild to moderate dyslipidemia.
Study Hypothesis: Daily consumption of almonds over 16 weeks will produce a decrease in hemoglobin A1c (HbA1c) levels in adults with pre-diabetes. Lay Summary: Persons developing type 2 diabetes mellitus (T2DM) will typically first have a condition called pre-diabetes. Lifestyle is a major factor that determines whether pre-diabetes becomes full T2DM. Lifestyle includes dietary habits and physical activity. Many people develop T2DM because of poor dietary habits and a sedentary lifestyle. Moreover, eating a high-fat, high-sugar diet can damage the blood vessels and increase the risk of strokes and heart attacks. A person's diet may produce substances in the blood that can interfere with the production of insulin in the pancreas. Sometimes, these changes in the insulin producing cells are serious and can eventually interfere with how the cells in the body use blood sugar, which causes T2DM. Techniques are available to measure circulating substances in the blood of persons with pre-diabetes that may be associated with the development of T2DM. Laboratory research has shown that almonds contain high levels of important compounds that may influence the onset of heart disease and T2DM. A meal plan that includes almonds daily will be given to half of the study participants and the other participants will be given a meal plan that is "nut-free". Because of the potential to delay the onset of heart disease and T2DM in some persons with pre-diabetes, this 16-week study will collect and analyze blood samples for changes that may make the person with pre-diabetes more likely to develop heart disease and T2DM. Blood samples will be collected at weeks 0, 8 and 16 to measure compounds that may be influenced by consuming almonds daily. This study will also attempt to understand other possible causes of heart disease and T2DM in persons with pre-diabetes; particularly those that might be related to body weight and body composition. Body composition techniques using very small amounts of electrical current are available to study body fat. Body weight, waist and hip measurements, blood pressure and body composition testing will be performed at the start of the study and every 4 weeks during the study. Lastly, these other possible causes of heart disease and T2DM will be investigated to look at relationships with the substances in the blood.
Offspring of patients with type 2 diabetes have increased risk of developing diabetes and are typically more insulin resistant than their peers with no diabetes family history. We have recently demonstrated that, in contrast to their sedentary counterparts, physically active offspring are not insulin resistant. In the proposed controlled clinical study, we will examine the effects of a moderate exercise programme on insulin resistance, and other metabolic risk factors, in sedentary offspring and matched control subjects. We hypothesise that offspring will exhibit an augmented response to exercise, thereby normalising their predisposition to an adverse metabolic profile. We will also investigate expression of adipokines and other genes in adipose tissue to determine whether these contribute to the increased insulin resistance observed in offspring and whether they are influenced by exercise. The results will help to determine the efficacy of exercise in normalising metabolism in offspring and will help elucidate the mechanisms involved.
The prevalence of type 2 diabetes is rising in the population for many years. It is now recognized that a period of glucose intolerance precedes the clinical symptoms appearance. This is due to a combination of b-cell dysfunction and insulin resistance. It is estimated that this pre-clinical phase of type 2diabetes may antedate the onset of overt diabetes by 10-12 years. Furthermore, insulin resistance is considered to be a main component of the metabolic syndrome and associated with significant cardiovascular morbidity and mortality. Recently, there has been an effort to pinpoint the pre-diabetic phase for early therapeutic intervention in the individual. These studies, in patients with impaired glucose intolerance, have shown to be beneficial from both lifestyle change and pharmacological intervention. It is thus hypnotized that intervention in patients with insulin resistance with or without glucose intolerance may prevent the progress of type 2 diabetes and it’s complications. There is difficulty in identifying individuals who are at high risk for type 2 diabetes. The prevention strategy relies on intervention in a pre-diseased state. In the case of type 2 diabetes, the early intervention is useful in the phase where there is insulin resistance, but prior to the appearance of glucose intolerance. The diagnosis of insulin resistance is a challenging one. The gold standard in diagnosing insulin resistance is the hyperinsulinemic-euglycemic clamp, but this method is not suitable for routine clinical use. Thus, less invasive methods for evaluation, like homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI), were developed. There is a correlation between HOMA and QUICKI results and the hyperinsulinemic-euglycemic clamp. Both HOMA and QUICKI allow insulin resistance diagnosis. The results from those tests correlate with hyperinsulinemic-euglycemic clamp and allow diagnosing insulin resistance, however, those indexes require serum glucose, insulin measurements and quite complicated calculations. A new method was suggested, non-invasive, sensitive and simple, for the identification of insulin resistance. In normal individuals, in the presence of insulin, glucose is taken up by a variety of cells, undergoes glycolysis and enters the tricarboxylic acid cycle or fat synthesis. In either case, CO2 in produced as a by-product. This CO2 enters the circulation and is discarded by the lungs. The new method is based on the assumption that 13C-glucose is ingested as described and its by-product 13CO2 can be measured in the expired air. In type 2 diabetes and other states of insulin resistance glucose, uptake is impaired and results in blunted 13CO2 production. This hypothesis was tested by Lewanczuc et al. The writers compared the [13C]-glucose breath test with hyperinsulinemic-euglycemic clamp, HOMA and QUICKI indexes. They tested 26 patients at different stages of insulin sensitivity and reported a good correlation of the glucose breath test and the other indexes. We suggest testing a larger group of patients at high-risk to develop type 2 diabetes and compare the glucose breath test with HOMA index.
The purpose of this study is to determine if, in men and women with excess abdominal fat and insulin resistance, people with HIV infection respond differently than people without HIV to interventions that typically improve body fat distribution and insulin resistance. The specific interventions are: 1. Diet + exercise program. 2. Rosiglitazone treatment. 3. A combination treatment of diet + exercise program and rosiglitazone.
The purpose of this study is to determine the mechanisms by which HIV protease inhibitors contribute to the development of diabetes in HIV-infected patients. The investigators propose that some HIV protease inhibitors impair insulin secretion and increase the production of glucose by the liver.