View clinical trials related to Insulin Resistance.
Filter by:Hypovitaminosis D is highly prevalent in the general population, particularly in obese individuals. Besides being associated with obesity, vitamin D deficiency seems to be involved in the pathogenesis of insulin resistance and low-grade chronic inflammation. In addition, it has been reported that individuals with low vitamin D levels are at increased risk for cardiovascular diseases. A healthy diet and weight loss are cornerstones in the prevention of cardiovascular diseases. Vitamin D supplementation could increase the beneficial effects of these lifestyle interventions. The purpose of this study is to assess whether vitamin D supplementation in conjunction with a hypocaloric diet improves the cardiometabolic profile of overweight/obese subjects to a greater extent than diet alone.
America's preferential consumption of high-fat/high-sugar foods is a driving force in the current epidemic of obesity and insulin resistance. Recent scientific observations suggest that the taste of food may play a role in how the body processes the food eaten in a meal. The intestine may play a central role in all aspects of dietary fat metabolism, from initial encounter with taste buds in the mouth to eventual triglyceride (TG) storage in the body. The investigators hypothesize that elevated blood fats in insulin resistance are a result of elevated intestinal-TG secretion and poor communication of this organ to the rest of the body after meals. In this study, meal feeding and sensory studies will be performed to determine whether the mechanism of taste-associated intestinal signaling leads to higher levels of blood fats after meals in 24 healthy, insulin resistant and type 2 diabetic subjects. Individuals will consume special meals the night before the tests and participate in sensory tests in the morning to analyze the effect of taste. The goal of this work is to understand how insulin resistance may cause impaired signaling between the taste buds and the intestine to result in an elevation in blood lipids, which increases the risk for other chronic diseases. This study will generate data for a future study to understand how diabetes treatment affects this process.
Metabolic syndrome (MS) is a cluster of risk factors for cardiovascular disease with increasing prevalence worldwide and insulin resistance is central to its pathophysiology and multi-organ deleterious effects. One of the most affected organs, the heart, undergoes a remodeling process with an increase in fibrous tissue that impairs global cardiac function. Considering that myocardial fibrosis increases myocardial stiffness, one important determinant of diastolic function, it probably contributes decisively to subclinical left ventricular diastolic dysfunction (DD) and heart failure with preserved ejection fraction in patients with MS. Since insulin resistance is a dominant player in the pathophysiology of MS, improvement of the metabolic profile of these patients with metformin might be associated with favorable remodeling of myocardial structure and an improvement in myocardial function. Metformin is a widely used drug to treat type 2 diabetes mellitus and is considered an option in the treatment of high-risk non-diabetic patients with MS, in addition to lifestyle counseling including a healthy diet and physical activity. In this way, we aim to: i) assess if treating non-diabetic patients with MS and DD with metformin in addition to lifestyle counseling decreases cardiac fibrosis and improves diastolic function and assess its impact in functional capacity and health-related quality of life (HRQoL); ii) evaluate if biomarkers of cardiac remodeling and inflammation are predictive factors of response to metformin treatment in these patients. This is a prospective, randomized, open-label, blinded-endpoint (PROBE) trial (scheduled follow-up of 24 months) with 2 arms: lifestyle counseling only and lifestyle counseling plus metformin (maximum dose of 1000mg twice daily). The primary endpoint will be change in change in mean of septal and lateral early diastolic mitral annular velocities (E') (at the end of the 24 months of follow-up). The secondary endpoints will include a composite of major cardiovascular events; diastolic function parameters at rest; plasma levels of insulin, glucose, insulin resistance index, NTproBNP, high-sensitivity C-reactive protein, tumor necrosis factor-α (TNFα), tissue inhibitor of matrix metalloproteinase type 1 (TIMP1) and growth differentiation factor-15 (GDF-15); functional capacity; epicardial, pericardial and abdominal adipose tissue volumes, and coronary calcium score; HRQoL.
People who are overweight and/or obese are at risk of insulin resistance and type 2 diabetes. However, research has shown that some overweight and/or obese individuals remain insulin-sensitive and metabolically healthy despite their unhealthy body weight. The investigators hypothesise that overweight and/or obese people who were deemed insulin-sensitive in previous studies will maintain their insulin sensitivity and metabolic health over time. The investigators also hypothesise that the preservation of insulin sensitivity will be accompanied by key metabolic health markers.
The purpose of this study is to describe insulin resistance in a general chronic heart failure population, in combination with muscle strength, body composition and cardiac function. It is assumed that insulin resistance is increased in CHF patient, and that this is related to decreased muscle strength and decreased lean tissue mass.
The objective of this study is to determine the effects of cholecalciferol treatment on inflammation and insulin resistance, in patients on hemodialysis that are previously treated with paricalcitol. Cholecalciferol is produced by the action of sunlight on a cholesterol precursor in the skin. This compound is then converted to calcidiol (25(OH) D3) in the liver, whereupon calcidiol is converted in the kidney to calcitriol (1,25(OH)2D3), the active form of vitamin D. However, recently it has been shown that deficiency of either calcidiol or calcitriol is associated with inflammation, insulin resistance and increased mortality in the general population. Furthermore, when both calcidiol and calcitriol were deficient, the mortality risk was much higher than the deficiency of either alone. A possible explanation is that some of the non-renal tissues might critically depend on the endogenous conversion of calcidiol to calcitriol and not on circulating levels of calcitriol. Thus, low circulating levels of calcidiol might be associated with tissue level functional calcitriol deficiency despite adequate circulating levels of calcitriol. Therefore, the hypothesis is that: 1. In non-diabetic hemodialysis (HD) patients treated with therapeutic doses of paricalcitol (an analog of calcitriol), calcidiol deficiency is associated with inflammation and insulin resistance and 2. In calcidiol deficient, non-diabetic HD patients with inflammation and treated with therapeutic doses of paricalcitol, cholecalciferol will reverse the calcidiol deficiency and thereby, reduce inflammation and insulin resistance. Interleulin-6 (IL-6) is thought to play a central role in insulin resistance by down-regulating glucose transporter-4 messenger RNA. Furthermore, IL-6 levels are significantly negatively associated with calcidiol levels, therefore will be measured as the primary outcome.
Obesity is an epidemic in Western society and is the biggest risk factor for insulin resistance and type 2 diabetes. The investigators have recently shown that exposure to hyperbaric oxygen (HBO) leads to an increase insulin sensitivity in males ubjects and that this improvement can be measured in all men, not just those with diabetes. The aim of this study is to investigate the time course of this effect and explore the mechanisms involved. The investigators suspect that insulin sensitivity as measured by hyperinsulinaemic-euglycaemic clamp will be increased within the time-frame of one 2-hour hyperbaric oxygen exposure, and that the improvement will be measurable in females as well as males.
The purpose of this study is to assess changes from baseline in insulin sensitivity, hepatic fat content and beta cell function after approximately 24-25 weeks of treatment with canagliflozin compared to placebo in participants with type 2 diabetes mellitus (T2DM) with inadequate glycemic (blood sugar) control on metformin monotherapy or on combination therapy with metformin and a dipeptidyl peptidase-4 (DPP-4) inhibitor.
Several studies showed that hyperuricemia is an independent risk factor for development of diabetes mellitus. However none of the previous studies have investigated the effect of lowering serum uric acid levels on insulin resistance of which is also named as prediabetes. With this background in mind, we aimed to test the effect of lowering serum uric acid level with allopurinol on insulin resistance.
This research is to investigate the nutritional supplement chromium picolinate. The investigators are testing to see how effective this supplement is in treating insulin resistance associated with HIV disease.