View clinical trials related to Insulin Resistance.
Filter by:Prediabetes is a term that refers to alterations in glucose homeostasis, including impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or both, involving a higher risk of progression type 2 diabetes mellitus (T2DM). Dapagliflozin is a selective and reversible inhibitor of sodium-glucose type 2 (SGLT-2) co-transporter, which reduces renal glucose reabsorption and promotes the glucose excretion through urine, so that the blood glucose is improved in patients with T2DM. Although this mechanism is independent of insulin, there are evidence of improved secretion and insulin sensitivity, so it is interesting to assess these effects in patients with prediabetes, as potential therapy for treating such disorders and prevent progression to T2DM. The aim of this study is to evaluate the effect of Dapagliflozin on insulin secretion and insulin sensitivity in patients with prediabetes. The investigators hypothesis is that the administration of dapagliflozin improve insulin secretion and insulin sensitivity in patients with prediabetes.
In addition to its role as the major regulator of glucose uptake into peripheral tissues, the hormone insulin is also a primary regulator of fat storage and fat burning of the body. Mechanistic animal studies have shown that high insulin may be the initial trigger for weight gain and be the proximal cause of obesity. There is currently no quick or non-invasive way of measuring insulin as research and clinical techniques require collection of a blood sample followed by a complicated and costly biochemical assay. The investigators will test the hypothesis that insulin levels can be accurately measured in saliva in humans following meals that elicit high and low blood insulin responses. Findings will help determine if insulin can be use as a valid fluid to track insulin changes in humans.
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.
Metabolic problems represent one of the major health concerns which are attractive for being addressed by nutritional interventions, as these are directly connected to dietary habits.Anthocyans possess cardiovascular disease prevention, obesity control, and diabetes alleviation properties, but association between anthocyans and prediabetes need to be more firmly understood and established from robust clinical data. However, there is little human research that has reported on the efficacy of increased anthocyans bioactive consumption on insulin sensitivity in pre-diabetes.
The aim of this study is to determine whether carnosine supplementation in overweight/obese individuals can improve insulin secretion and/or insulin resistance by decreasing sub clinical inflammation. The investigators hypothesise that carnosine supplementation will reduce type 2 diabetes and cardiovascular risk factors by lowering chronic low-grade inflammation (CLI), oxidative stress, advanced glycation end products (AGEs), and advanced lipoxidation end products (ALEs). Aim :To determine the capacity of carnosine supplementation to decrease major risk factors for type 2 diabetes and cardiovascular disease and identify metabolic pathways involved, specifically by: 1. Reducing diabetes risk (insulin sensitivity; secretory function and glucose tolerance) 2. Improving cardiovascular risk factors (lipids; arterial (aortic) stiffness; central blood pressure (cBP); endothelial function). 3. Decreasing the CLI, oxidative stress, AGEs, and ALEs, and increase detoxification of reactive carbonyl species (RCSs).
Branched-chain amino acids (BCAA) belong among nutrients strongly linked with insulin sensitivity (IS) measures. Their exact effect on IS appears to be dependent on various conditions that remain to be better defined . The aim of the current study was to investigate effects of chronic increase of BCAA intake on IS in two groups of healthy subjects differing in their basal consumption of BCAA, i.e. vegans and omnivores. Interventional trial was designed where vegans and omnivores were separately interveined with 15 (women) or 20 (men) grams of BCAA daily. Examinations of participants are intended to be done at baseline, after the intervention and wash-out period. Examinations (anthropometry, hyperinsulinaemic-euglycaemic clamp, arginine test) and blood analyses will be performed at baseline, after the intervention and after a 6 month wash-out period. Samples of subcutaneous abdominal adipose tissue (AT) and skeletal muscle (SM, vastus lateralis) obtained before and after the intervention will be used for various analyses (mRNA levels of selected metabolic markers, fatty acid composition, mitochondrial activity).
The purpose of this study was to determine whether dual treatment with metformin and alogliptin is more effective than treatment with metformin, alogliptin and pioglitazone in the treatment of obese women with polycystic ovary syndrome (PCOS) regarding insulin resistance and beta cell function.
An intermittent energy restricted (IER) diet may modify cardio-metabolic disease risk factors compared to an energy-matched continuous energy restricted (CER) diet. A randomised controlled parallel design trial will determine the impact of a short-term IER diet (2 consecutive days of very low calorie diet (VLCD), 5 days moderate energy restriction each week for a 4 week period), compared to a CER diet, on insulin sensitivity in healthy (disease-free) subjects with central obesity.
A PRoBE design study will be used to obtain saliva from patients before undergoing blood study evaluation for screening at risk patients for the presence of undiagnosed pre-diabetes of type II diabetes. Pre-specified saliva biomarkers will be evaluated along with multi-marker models for their discriminatory value for distinguishing patients with normal glucose metabolism from those with disease. Appropriate housekeeping genes will also be incorporated to allow for the measurement of relative gene expression.
Our studies are aimed at examining effects of intrauterine exposure to GDM on metabolic risks in Hispanic children. Our primary hypothesis predicts that intrauterine exposure to GDM will be associated with one or more of three critical factors involved in the development of diabetes: 1) increased adiposity, 2) insulin resistance, and 3) decreased beta cell function in Hispanic children when compared to non-exposed children matched for ethnicity, age, gender, and Tanner stage. In a subset of this cohort, we will also examine the effects of intrauterine exposure to gestational diabetes on the brain pathways that regulate appetite and body weight in children ages 6 to 15 years old.