View clinical trials related to Insulin Resistance.
Filter by:The goal of this study is to collect more information from people with plaque psoriasis and to determine if insulin plays a role in the pathogenesis of psoriasis. The main question it aims to answer is if insulin action is preserved or even enhanced in psoriatic lesions despite insulin resistance elsewhere. Participants with plaque psoriasis will have punch biopsies taken of lesional and non-lesional skin after an overnight fast and then during an oral glucose tolerance test. Biopsy specimens will then be assessed for markers of insulin action.
Diabetes mellitus (DM) is a complex chronic illness associated with a state of high blood glucose level, or hyperglycemia, occurring from deficiencies in insulin secretion, action, or both. Diabetes mellitus is the name given to a wide spectrum group of disorders characterized by raised plasma glucose.Type 1 diabetes is characterized by an absolute insulin deficiency due to autoimmune destruction of insulin producing beta cells in the pancreas. most adults with diabetes have type 2, characterized by a relative insulin secretory defect, and target tissue resistance to the effects of insulin.
In humans, insulin is secreted in pulses from the pancreatic beta-cells, and these oscillations help to maintain fasting plasma glucose levels within a narrow normal range. Given the fluctuations in insulin concentrations, oscillations enhance precision of control. The hyperinsulinemic euglycemic clamp test (clamp) involves a continuous infusion of insulin and is the gold standard for measuring insulin sensitivity. In this study, insulin sensitivity measured using the standard clamp will be compared with a clamp in which the same total amount of insulin as the standard clamp is infused every five minutes instead of continuously.
Type 2 diabetes is the most common metabolic disease worldwide, characterized by hyperglycemia, decreased whole body insulin sensitivity, and white adipose tissue (WAT) dysfunction. A key factor in its development is chronic overnutrition, usually with a high-fat diet (HFD), leading to disturbances of glucose and lipid metabolism. However, the mechanism of short-term HFD-induced tissue-specific insulin resistance remains poorly understood. This project aims to further unravel the underlying mechanisms of short-term HFD overnutrition-mediated WAT insulin resistance. The model described here corresponds to a randomized, single- blinded parallel-grouped trial, consisting of two interventions: a macronutrient-balanced diet and or a hypercaloric diet over three weeks in order to investigate differences in interorgan fatty acid and glucose metabolism between the studied groups. Based on recent studies, the hypothesis is that 21-day hypercaloric HFD induces WAT insulin resistance via a diacylglycerol, novel protein kinase C-insulin receptor signaling model in both fasting and insulin-stimulated states.
The overall goal is to determine how a sleep extension intervention (increasing time in bed) in individuals who maintain less than 6.5 hours sleep per night affects their plasma ceramides and insulin sensitivity. Participants will undergo a randomized controlled trial, with sleep extension (intervention) and healthy lifestyle (control) groups. The sleep extension is designed to increase participant's time in bed by 2 hours per night. Alternatively, the control group will receive basic health information (e.g., physical activity, goal setting, and nutrition when eating out).
The proposed research is designed to extend previous research findings building on the knowledge of strawberries as fruits that support a healthy immune and vascular system. The proposed research leverages a recently funded proposal by the USDA to study in greater depth inflammation, glucoregulation and oxidative stress defense and their relation to improving endothelial function and insulin sensitivity. Before and after strawberry intake, blood samples will be collected for monocyte (immune cells and source of inflammatory cytokines) isolation and activation via changes in cellular NF-κB and Nrf-2 (key transcription factors of inflammation/oxidative stress defense) status along with products of their activation (ie., plasma cytokines). Because inflammation and oxidative stress impairs endothelial function and insulin sensitivity, acutely and chronically, investigators will also study changes in vascular and insulin sensitivity status, assessing changes in vascular adhesion molecules, endothelial responsiveness through flow mediated vasodilation (ie., FMD) and insulin sensitivity using the Liquid Meal Tolerance (LMTT) if intravenous glucose tolerance test (IVGTT) method cannot be used due to supply chain issues of sterile Dextrose. Glucoregulation will be assessed by placing a Continuous Glucose monitoring (CGM) machine (Dexcom-6) to participants for 10 days at the beginning and at the end of the study period of intervention. The study will be a randomized, double-blinded, 3-arm parallel, 4-week, dose-response study. Individuals with chronic low grade inflammation will be sought to test the anti-inflammation - vaso-relaxing - insulin sensitivity effects of strawberry.
Enrolling of 150 female patients of fertile age diagnosed with PCOS, insulin resistance, infertility, or mitochondrial disease, and the same number of age- and sex-matched controls are planned. During the research biomarkers already with mitochondrial dysfunction in the scientific literature and common mtDNA abnormalities (deletions, point mutations, copy number changes, etc.) are examined.
Effects of insulin resistance in non-diabetic acute coronary syndrome patients by the homeostasis model assessment index (HOMA2-IR)
The goal of this intervention study is to learn about how weight loss impacts molecular signaling of intermuscular adipose tissue (IMAT) in individuals with obesity. The main question it aims to answer is how inflammatory molecules secreted by IMAT promote muscle insulin resistance and inflammation, and how these same molecules are diminished after weight loss. Following screening visits involving body composition measures, blood testing, strength testing, and a thigh muscle biopsy, participants will go through a 12-week dietary intervention for weight loss. After 12 weeks, this will be followed by the same testing and biopsies that were completed before the intervention. Researchers will then compare outcomes of individuals who lost weight to individuals who did not lose weight.
Alzheimer´s disease (AD) is the most common cause of dementia. The most important risk factor for AD is old age; modifiable risk factors for AD include metabolic risk factors, i.e. diabetes, and obesity. Insulin resistance seems to be associated with AD pathology and cognitive decline. Previous studies suggest that AD and mild cognitive impairment (MCI) due to AD, a stage between normal cognition and AD dementia, would be associated with central nervous system (CNS) insulin resistance. Insulin resistance can be measured using a sophisticated hyperinsulinemic-euglycemic clamp technique. Insulin-stimulated glucose uptake of muscles and adipose tissue is known to be reduced in an insulin resistant subject compared to healthy insulin sensitive subjects. Central nervous system insulin resistance, however, is more difficult to assess, while a clear-cut definition is thus far lacking. Previous studies have demonstrated that whole-body insulin resistance in obese subjects is accompanied with higher brain glucose-uptake (BGU) during the insulin clamp, compared to lean controls, and that BGU increases from the fasting to the insulin clamp state. On the contrary, there is no difference in BGU under fasting conditions between obese subjects and healthy lean controls. No previous studies have evaluated brain glucose uptake in clamp conditions in subjects with MCI or early AD. The aim of this study is to evaluate if brain glucose uptake is increased in MCI/ early AD subjects in a similar manner as in morbidly obese subjects in an insulin-stimulated state (during a hyperinsulinemic clamp) when compared to the fasting state, and when compared to controls. The investigators hypothesize that MCI subjects would have CNS insulin resistance that could, in time, contribute to the pathological process of AD. The investigators will recruit altogether 20 MCI subjects from the local memory clinic, and healthy controls through advertisements. All participants will undergo two [18F]-fluorodeoxyglucose (FDG) positron emission tomography (PET) scans (one in the fasting state and one during the hyperinsulinemic clamp), a magnetic resonance image scan for structural changes, blood sampling, and comprehensive cognitive testing. The participants will also undergo a [11C]PIB-PET scan to measure brain amyloid accumulation. Understanding the metabolic changes in the brain preceding AD could help in developing disease-modifying treatments in the future.