Active clinical trials for "Insulin Resistance"

Resistance to the hypoglycemic action of insulin develops within 7 days of bedrest in young, healthy volunteers. We propose that the same event occurs in elderly individuals confined to bed, that alterations in lipid metabolism are, at least in part, responsible for the insulin resistance associated with bedrest, and that the accumulation of intracellular triglyceride (TG) in liver and muscle will play a role in impairing insulin action. Further, we propose that the PPARα (Peroxisome Proliferator-Activated Receptor Alpha) agonist fenofibrate will increase tissue fatty acid disposal by activating mitochondrial oxidative capacity, thereby improving insulin sensitivity. We will investigate a series of specific hypotheses designed to examine the role of altered lipid metabolism in the development of insulin-resistance associated with bedrest. Further, since inactivity is likely a principal factor in the development of insulin resistance in the elderly, the response to the inactivity imposed by bedrest represents an acceleration of the normal development of insulin resistance in elderly individuals. Therefore, the results of this study will also be pertinent to the understanding of the mechanisms responsible for the natural development of insulin resistance in free-living elderly.

This study is being done to find out if participants with insulin resistance and hepatitis C virus genotype 1 (HCV GT1) infections who failed dual therapy with peginterferon alfa (PegIFN) + ribavirin (RBV) will benefit from the addition of boceprevir to PegIFN + RBV (triple therapy).

The aim is to continue our program on PDE5 inhibition by evaluating effects on insulin resistance, including glucose metabolism and subclinical inflammation, after a 6-week administration of tadalafil in T2D patients. The primary objective is to study the effect of tadalafil compared with placebo on insulin sensitivity during a euglycemic hyperinsulinemic clamp. This is a double-blind, placebo-controlled crossover study with one study site. Twenty-five T2D patients will be recruited and randomized to per oral intake of tadalafil 20 mg o.d. for six weeks and after a wash-out period of eight weeks intake of placebo for another six weeks, or vice versa. At the end of each 6 week treatment period a glucose clamp, subcutaneous needle biopsies as well as muscle and subcutaneous microdialysis will be performed. Endothelial function tests and arginin stimulation of insulin secretion tests will be performed after 3 weeks in each treatment arm.

During this project the investigators will evaluate whether the effects of arabinoxylan oligosaccharides (AXOS) consumption on insulin resistance in participants with metabolic syndrome can be explained by the production of short-chain fatty acids (SCFA). Secondly, the investigators will evaluate whether changes in gut hormone production might explain the effect on insulin resistance.

In this study investigators will compare the health effect of two different meal patterns. In one, participants will consume food according to an 'irregular meal pattern' (minimum 3 meals, maximum 9 meals per day) and in the other 'regular meal pattern' (6 meals per day) for two weeks. The energy requirement of the participants will be calculated to maintain body weight during the study. Participants will be provided with all the food to be consumed during the study. Initially, interested individuals will attend a screening visit in which they will complete questionnaires on medical health, eating habits and physical activity. Height, weight and waist circumference will be measured at this visit. Thereafter, participants will be assigned to a 2-week period following one of the two meal-patterns. There will be a 2-week period between the two interventions when they will consume their normal diet and at the end of this, participants will undertake the next meal pattern. During the two phases participants will be asked to wear an armband (which detects movement and measures heat loss), to assess their energy expenditure and an interstitial glucose monitoring device will be worn for seven days. Before and after each 2-week intervention, participants will come to the laboratory for a mixed-meal tolerance test. Blood samples will be obtained before and for 3hrs after eating to evaluate the health effects of the meal patterns. Energy expenditure will be measured by ventilated-hood indirect calorimetry and the armband device. At the end of the 3hr post prandial period, participants will be offered an ad libitum pasta lunch and be asked to eat until they feel comfortably full. During each of the 2-week periods, participants will be asked to record their food intake and record their appetite sensations on specific days.

Insulin promotes the clearance of sugars from the blood into skeletal muscle and fat cells for use as energy; it also promotes storage of excess nutrients as fat. Type 2 diabetes occurs when the cells of the body become resistant to the effects of insulin, and this causes high blood sugar and contributes to a build-up of fat in muscle, pancreas, liver, and the heart. Understanding how insulin resistance occurs will pave the way for new therapies aimed at preventing and treating type 2 diabetes. Mitochondria are cellular structures that are responsible for turning nutrients from food, into the energy that our cells run on. As a result, mitochondria are known as "the powerhouse of the cell." Mitochondria are dynamic organelles that can move within a cell to the areas where they are needed, and can fuse together to form large, string-like, tubular networks or divide into small spherical structures. The name of this process is "mitochondrial dynamics" and the process keeps the cells healthy. However, when more food is consumed compared to the amount of energy burned, mitochondria may become overloaded and dysfunctional resulting in a leak of partially metabolized nutrients that can interfere with the ability of insulin to communicate within the cell. This may be a way for the cells to prevent further uptake of nutrients until the current supply has been exhausted. However, long term overload of the mitochondria may cause blood sugar levels to rise and lead to the development of type 2 diabetes. This study will provide information about the relationship between mitochondrial dynamics, insulin resistance and type 2 diabetes.

The purpose of the study is to develop a culturally adapted intervention (CAI) program to improve weight and physical activity in overweight or obese adult Latinos at high risk for developing type 2 diabetes and/or cardiovascular disease (CVD) and to rigorously evaluate the effectiveness and implementation potential of the CAI program.

The purpose of this study is to determine the key factors influencing insulin sensitivity in type 1 diabetes (T1DM) and maturity onset diabetes of the young, type 2 (MODY2). Our study tests the hypothesis that decreased insulin sensitivity is primarily driven by chronically elevated insulin levels in the blood rather than chronic elevations in blood sugar.

The aim of the study will investigate whether impairment in the action of insulin to promote the use of glucose in skeletal muscle (insulin resistance) as a result of oral ingestion of a liquid meal rich in saturated fat is linked to reduced ability of muscles to synthesise new protein in response to dietary protein intake, which ultimately may compromise maintenance of muscle size and quality of life and whether partially replacing saturated fat in the liquid meal with omega 3 polyunsaturated FA (n3PUFA) will ameliorate these negative effects.

The purpose of this study is to assess the safety, tolerability, and the effect of food on KQ-791. Each participant may receive up to 3 single doses of KQ-791 (at up to 3 different dose levels) and 1 placebo dose over the course of the study. Up to 6 escalating dose levels may be studied, in two distinct groups or cohorts.