View clinical trials related to Insulin Resistance.
Filter by:The purpose of this study is to investigate the effects of 5 weeks treatment with dapagliflozin in type 2 diabetes patients on how the hormone insulin acts on sugar uptake in muscles.
Accumulation of intramyocellular lipids (IMCLs) due to increased supply of fatty acids can induce defects in the insulin signaling cascade, causing skeletal muscle insulin resistance. However, the causes for muscle insulin resistance are not well understood. The association of elevated IMCLs and insulin resistance has been shown in obese humans and individuals with type 2 diabetes as well as several animal models of insulin resistance. Despite the strong relationship between IMCLs and insulin resistance, this suggested relationship disappears when well-trained endurance athletes are included into this consideration as this group is highly insulin sensitive. This metabolic enigma has been termed the 'athlete's paradox'. The aim of this project is to resolve the mechanisms contributing to the athlete's paradox.
The aim of the study is to describe an immune activation profile of people at risk of insulin resistance based on a wide range of markers which will allow easy identification of patients at risk.
This is a family based genotype-phenotype study designed to assess genetic and environmental influences on obesity, insulin resistance and beta cell function in the context of gestational diabetes.
The purpose of this randomized study is to assess the efficacy of a mobile application for the improvement of blood pressure and insulin resistance in people with metabolic abnormalities.
Chronic spinal cord injury (SCI) results in adverse soft tissue body composition changes and an extremely sedentary lifestyle. These abrupt changes often lead to a high prevalence of cardiometabolic diseases, such as impaired glucose tolerance/diabetes mellitus and dyslipidemia, conditions which predispose those with SCI to an increased risk for cardiovascular disease compared to the general population. Due to paralysis and wheel chair dependence, maintaining an adequate level of physical activity to counteract these deleterious metabolic changes presents a unique obstacle because conventional first line interventions are lifestyle modifications (e.g., diet and exercise), which may be difficult to achieve. Recently, a new medication has been approved by the Food and Drug Administration to improve glycemic control in individuals with diabetes mellitus, and it has also been investigated as an off-label treatment to induce weight loss. Glucagon-like peptide-1 (GLP-1) agonists are a class of drugs designed to mimic the endogenous incretin hormones released from the gut in a glucose dependent manner following a meal. The mechanisms of action for this drug class of medications include stimulation of glucose-dependent insulin secretion, inhibiting glucagon release, slowed gastric emptying, and reduction of postprandial glucose excursions following food intake. In addition to improved glycemic control, this class of medications also shows promise for its non-glycemic action of facilitating weight loss. The method of delivery of the GLP-1's is by self-administered injections once daily or once weekly, depending on the severity of the clinical case and therapeutic targets for a specific patient.
The investigators are trying to understand the role of DNA (deoxyribonucleic acid) methylation in insulin resistance in skeletal muscle and blood tissues. DNA methylation is a normal chemical process in the body that modifies DNA. By studying this, the investigators hope to better understand the causes of insulin resistance.
Around the world, the prevalence of type 2 diabetes mellitus (T2DM) has been increasing since the last two decades, with approximately 347 million patients with diabetes by 2013 according to the World Health Organization (WHO). This pronounced increase is due to an increase in the prevalence of obesity, reduction in physical activity levels, accelerated urbanization and aging of the population. In Colombia, T2DM ranks fifth in the main morbidity and mortality causes, including only deaths caused directly and without adding the strong influence that T2DM has on cardiovascular disease mortality. Insufficient tissue response to normal insulin concentrations, called insulin resistance, is one of the central pathophysiological mechanisms in the development of T2DM. However, there is currently no simple, practical, safe and reproducible method that allows the diagnosis or identification of insulin resistance, nor the follow-up to its evolution. At the moment, the gold standard for assessing the degree of insulin sensitivity or resistance is the "hyperinsulinemic-euglycemic clamp", a laborious technique, of high cost and high technical difficulty, requiring specialized personnel and hospitalization. Non-invasive methods based on mathematical regressions, such as the Homeostatic Model Assessment (HOMA-IR), are imperfect and widely variable, and have not been validated in the Latin American population, less Still Colombian. Therefore, the development of new, easily obtainable quantitative tools for the diagnosis of insulin resistance is required. This requires not only the identification of new and better biomarkers, but also the determination of their diagnostic performance and operational characteristics. This project will investigate 3 molecular targets (myokines), novel and easy to measure, with high probability of being good biomarkers of insulin resistance. The research will include validation of its association with insulin resistance measured by the reference method, as well as its measurement in apparently healthy individuals. Finally, operator-receiver characteristics of each test will be analyzed, in order to propose a cutoff point for the diagnosis of insulin resistance.
This study will assess the feasibility of a randomized control trial in which the effects of probiotic supplementation throughout pregnancy on maternal insulin sensitivity and inflammation, as well offspring gene expression and body composition are examined.
The prevalence of overweight and obesity in Singapore is approximately half of that in the United States, yet the incidence of type 2 diabetes is similar, and is expected to double in the near future. This indicates that metabolic dysfunction, particularly insulin resistance, is widely prevalent even among individuals who are considered normal-weight or lean by conventional measures, i.e. body mass index (BMI) and percent body fat. These individuals are often referred to as "metabolically-obese normal-weight" (MONW), and have increased risk for cardiometabolic disease despite their normal BMI and total body fat values. The prevalence of the MONW phenotype varies across populations and differs markedly among different ethnicities. However, our understanding of the complex interactions between ethnicity, body composition, and metabolic dysfunction and its reversal remains rudimentary. Previous attempts to characterize the MONW phenotype are confounded by the small but significant differences in BMI or percent body fat between groups (even if all subjects were lean, within the "normal" range), with MONW subjects being always "fatter" than the corresponding control subjects. There are no published studies that prospectively recruited groups of metabolically healthy and unhealthy lean individuals matched on BMI and percent body fat. Furthermore, although weight loss improves body composition and many of the cardiometabolic abnormalities in most obese patients, little is known about the possible therapeutic effects of calorie restriction in MONW subjects. Accordingly, a better understanding of the MONW phenotype and the evaluation of therapeutic approaches for its reversal will have important implications for public health. By facilitating earlier identification of these subjects, who are more likely to go undiagnosed and thus less likely to be treated before clinically overt cardiometabolic disease develops, results from this study will allow for earlier and effective intervention.