Active clinical trials for "Insulin Resistance"

Obesity is an independent risk factor for type 2 diabetes and cardiovascular disease. The increased prevalence of obesity worldwide is a major concern among the scientific and medical communities. Insulin resistance is a common factor associated with obesity, metabolic syndrome, hypertension, and type 2 diabetes. Individuals affected by these conditions often experience endothelial dysfunction as well. Insulin resistance provides a key link between metabolic syndrome risk factors and vascular disease. Development of strategies aimed at preventing vascular dysfunction and future disease caused by metabolic disturbances is needed. Although the relationship between obesity and various diseases is well known, the acute effects of insulin on vascular function in obese individuals have yet to be fully determined. Additionally, the effects of acute exercise on insulin-stimulated endothelial function are unknown. Exercise may be an effective and potent treatment that protects against endothelial dysfunction, insulin resistance, and future cardiometabolic disease commonly present with obesity. However, less attention has been placed on vascular insulin sensitivity. The purpose of this study is to test the hypothesis that a single bout of exercise increases insulin-stimulated blood flow at the macro- and micro-vasculature level in obese individuals with metabolic syndrome to similar levels as healthy obese control. Our laboratory has available non-invasive methods to quantify vascular function and the gold-standard technique for assessing insulin sensitivity (euglycemic-hyperinsulinemic clamp). The investigators will assess vascular function (flow-mediated dilation, post-ischemic flow velocity and contrast-enhanced ultrasound) as well as arterial stiffness (augmentation index and pulse wave velocity) before and at the end of the clamp protocol performed the morning following a bout of exercise and a control (no-exercise) condition in 1) metabolic syndrome and 2) obese adults. If our hypothesis is sustained, it will suggest that a key role of the vasculature exists in regulating insulin following exercise and will provide insight into the link between the vasculature, obesity, metabolic syndrome and cardiovascular disease and may confer decreased risk for cardiometabolic disease.

Stunting is still a major problem in developing countries, including Indonesia, and has been associated with impaired development. Stunted children have also a higher risk of metabolic syndrome in adulthood. The gut microbiota, as a part of intestinal integrity, may promote intake of nutrient during childhood. Probiotics supplementation may optimize the balance of gut microbiota and further improve child growth during the window period. Furthermore, calcium could also improve child growth by increasing the resistance to intestinal infection. However, the long-term effects of gut microbiota optimization during childhood using probiotics and calcium on growth, development, and the metabolic condition has not widely studied.

The goal of this research study is to learn more about the hormones that muscles make during exercise, and if those hormones are associated with type 2 diabetes risk in adults who are overweight or obese. Participants will undergo exercise testing on an upright bicycle, with blood samples taken for muscle hormones before and after exercise. The hypothesis is that adults with overweight/obesity and insulin resistance will have an impaired muscle hormone profile in response to exercise compared to adults with overweight/obesity who are not insulin resistant.

This is a large and comprehensively phenotyped cohort with fasting glycaemia where the predictive value of body composition and anthropometric measures of total and central fat distribution for postprandial carbohydrate intolerance are studied.

Use of CGM to determine diagnosis in possible spontaneous or reactive hypoglycaemia. Use of CGM to aid treatment optimisation in spontaneous or reactive hypoglycaemia

The popularity of marathons and endurance events has increased over the last few decades and, interestingly, the demographics of participants have also changed. From 1980 to 2002 the average race time to complete the marathon lengthened from ~3.5 hours to ~4.5 hours. Likewise, many endurance races include "Clydesdale" and "Athena" divisions for heavier weight male and female runners, respectively. As such, there has been an increase of overweight and obese participants in these races. For example, one study consisting of 250 runners determined, according to BMI, that approximately 15% and 31% of the female and male participants, respectively, were classified as overweight, with 31% and 33% classified as obese. Therefore, many recreational endurance athletes are overweight despite their high level of activity. On one hand, these data are positive as regular exercise reduces cardiovascular disease and all-cause mortality in overweight and obese populations. Yet, it is well documented in sedentary obese individuals that excess adiposity can lead to disturbances in adipocyte lipolysis and altered substrate utilization at rest and during exercise, and can decrease muscle quality. However, it is unknown if overweight individuals that exercise regularly have disrupted fat metabolism, circulating hormones, or muscle quality. No study has directly determined if differences exist in fat metabolism, circulating hormones, and muscle quality between overweight recreational female athletes and their lean counterparts when training status is equivalent. Therefore, the purpose of this investigation is to determine if differences in pre and post-exercise fat metabolism, circulating insulin and growth hormone, and muscle quality exist between active overweight individuals compared to active lean individuals with similar training history and who have regularly trained for and participated in endurance events within the last few years.

Obesity is associated with low-grade inflammation, insulin resistance and low vitamin D status. Vitamin D has traditionally been known to involve in calcium homeostasis and prevent rickets; however, recently it has been recognized to inversely associate with many non-skeletal diseases and conditions including obesity and type 2 diabetes (T2DM). In vitro studies have demonstrated that vitamin D possesses anti-inflammatory properties. It remains unknown if the effect of vitamin D on insulin sensitivity is mediated by suppressing inflammation in human adipose tissues. The main objective of this study was to assess the association between vitamin D and insulin sensitivity and inflammation in morbidly obese pre-menopausal women. Obese women (n=76) were recruited from the University of Illinois at Chicago (UIC) Nutrition and Wellness Center and the UIC medical center bariatric surgery clinics. Insulin sensitivity/resistance was assessed by (1) Oral glucose insulin sensitivity (OGIS) index, derived from dynamic oral glucose tolerance test (OGTT), and (2) Homeostasis model of insulin resistance (HOMA-IR), calculated from fasting steady-state glucose and insulin. Also, to better understand the potential mechanism and the role circulating vitamin D (25OHD) plays in adipose tissue inflammation, we assessed messenger ribonucleic acid (mRNA) expression of vitamin D receptor (VDR) and various inflammatory genes in visceral (VAT) and subcutaneous adipose tissues (SAT) of obese women that underwent a restrictive bariatric procedure. We hypothesized that subjects with higher serum vitamin D levels would be less inflamed and more insulin sensitive and have increased expression of VDR and pro-inflammatory markers compared to those with lower serum vitamin D levels.

The (PYR1)-apelin-13 is an endogenous peptide discovered relatively recently (1998). The apelin and its receptor, which is named apj, are expressed in many tissues including sensitive to the action of insulin, such as skeletal muscle, adipose tissue and heart tissue. Recent work by the team of Prof. P.Valet (INSERM U1048, Toulouse) opened a new field of investigation, demonstrating for the first time in mouse models that apelin exerts a glucose-regulating in vivo action. The investigators propose a translational clinical research project whose goal is to provide the proof of concept of the favorable influence of apelin on insulin sensitivity in humans.

Sleep is an essential biological process for life and great value to functions such as learning, memory processing , cell and brain repair. Recently, new evidence points to the relationship between lack of sleep and carbohydrate metabolism , establishing a framework for insulin resistance observed in studies with restriction and sleep deprivation on several nights and in a single night . To reverse this process , one of the most effective strategies is physical exercise and part listed in the literature as a non-pharmacological tool for prevention and health promotion , as well as in the treatment of some diseases . However , the pace of modern society causes people to practice less physical exercise , lack of time being the main reason . In this scenario, the High Intensity Interval Training ( HIIT ) emerges as a powerful strategy that induces major changes optimizing the time spent on such activity. Considering the benefits of this mode , the purpose of this study is to investigate the effects of high-intensity interval training in the context of insulin resistance observed during sleep deprivation. Will be recruited 20 male volunteers, aged between 18 and 35 years old, healthy, with normal sleep duration equivalent to 7-8 hours / night, not smoking and regular eating habits. They will be submitted to a protocol of 6 sessions of high-intensity interval training for two weeks, and since the end period, sleep normally, or be deprived of sleep for 24 hours. Biochemical (thyroid hormones, cortisol, glucagon, free fatty acid, cholesterol, glucose and insulin) will be undertaken as well as evaluation of body composition by plethysmography, basal metabolic rate by indirect calorimetry and insulin sensitivity through Oral Glucose Tolerance Test (OGTT) before and after the training period.

Clinical and rodent studies have demonstrated the impact of specific dietary factors in modulating inflammation-related diseases including insulin resistance, type 2 diabetes, and cardiovascular disease. Such dietary factors include polyunsaturated fats, polyphenols, and glycemic index. The investigators know from previous studies in the literature that reducing the glycemic index and increasing the omega-3 fat and polyphenol content of the diet results in improved metabolic indices and reduced inflammation. These improvements can be observed even within the context of persistent obesity. The investigators will implement a reduced-calorie, multi-pronged dietary approach for improving insulin sensitivity and reducing inflammation in obese subjects with the metabolic syndrome. The active diet will include reduced glycemic index foods together with omega-3 fats and polyphenol supplements. The primary hypothesis is that the dietary combination of reduced glycemic index foods, omega-3 fats and polyphenols will work to reduce insulin resistance and inflammation more efficiently than a placebo-controlled, calorie- and macronutrient-matched diet in obese subjects with the metabolic syndrome.