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Atrial fibrillation (AF) is the most common arrhythmia worldwide. AF is associated with obesity and the co-morbidities of obesity, including hypertension and obstructive sleep apnea (OSA) which increase left atrial (LA) size and decrease LA function. Semaglutide, a Glucagon-like peptide receptor 1 agonist (GLP-1 RA), is currently approved by the Food and Drug Administration for weight loss for individuals with and without diabetes. The effects of pharmacologic weight loss with Semaglutide on AF are unknown. The investigators plan on conducting a randomized controlled trial of semaglutide versus placebo in individuals with paroxysmal or early persistent AF (>10% AF burden on ambulatory monitoring, a previous electrical cardioversion, or AF lasting ≥ 7 days but < 3 months who have a body mass index ≥ 27.0 kg/m2. The trial will last for 52 weeks. The primary outcome will be the change in AF burden for 2 weeks, immediately before starting the medication or placebo to two weeks starting at week 50, as determined by an implantable loop recorder or two week ambulatory Additional outcomes will be change in epicardial adipose tissue as determined by chest/abdomen/pelvis computed tomography scan at enrollment and at week 52, change in apnea-hypopnea index from baseline sleep study to week 52 sleep study, change in LA longitudinal strain from baseline echocardiogram to echocardiogram at 52 weeks, and change on symptom surveys.
This research project aims to investigate, in an innovative way, the molecular pathophysiology of gestational complications induced by maternal obesity and gestational diabetes mellitus (GDM). These complications have an immediate impact on obstetric outcomes - such as pre-eclampsia and intrauterine growth restriction - as well as long-term consequences for the health of the mother and child. This proposal aims to advance the understanding of the relationship between subclinical maternal and placental inflammation with dietary components through a prospective cohort of pregnant women. To this end, a prospective cohort of pregnant women will be conducted with four follow-up waves: 13th-20th (baseline), 24th-28th, 32nd-36th gestational weeks and at the time of delivery. Retrospective data referring to the first trimester of pregnancy will be obtained from the medical records. Pregnant women will be invited to participate in the study by registering at the prenatal service. Women who start prenatal care with less than 13 weeks of gestation will be registered, for capture in the 2nd consultation. The initial sample calculation is 120 volunteers. Maternal blood samples will be collected at 2 times: 2nd trimester appointment and 3rd trimester appointment. Placental and umbilical cord blood samples will be collected immediately after delivery. Dietary consumption during pregnancy will be assessed by 2 24-hour recalls at each visit (1 in person and 1 by telephone). The identification of functional biomarkers in maternal blood and placenta will serve for prognostic purposes of gestational complications such as Gestational Diabetes Mellitus. The identification of dietary factors associated with obesity and gestational diabetes mellitus and associated complications will provide information that will serve as a basis for nutritional guidelines for pregnant women.
This study is a 11 week telehealth intervention focusing on increasing physical activity in adolescents who are receiving medical care for obesity. The participants will be randomized into two groups: control and intervention. During the 11 weeks both groups will be contacted once a week for a video call. The control group will report their past week physical activity levels and the intervention group will review the material in weekly newsletters on behavior changes related to physical activity. Physical activity levels will be measures before and after the intervention.
The mechanisms regulating fat mass homeostasis are incompletely understood although recent animal and human trials would suggest that there is a leptin independent regulatory pathway which may play a role in weight control and maintenance. Although evidence would suggest that external loading in patients with obesity may promote body weight loss, this has not been explored in patients following bariatric surgery. The aim of this study is to investigate the mechanisms regulating weight loss and the potential role of the 'gravitostat' in fat free mass retention in patients following bariatric surgery.
Obesity is currently one of the most substantial health burdens. Due to the production of marked and sustained weight loss, bariatric surgery is an increasingly used therapeutic modality to combat obesity and its comorbidities. Surgical rearrangement of the gastrointestinal tract remarkably alters metabolism and hormones acting on neurological and hypothalamic signalling, involved in food decision-making and eating behaviour. In this context, many patients who underwent bariatric surgery self-report changes in appetite, satiety and food preferences. Furthermore, new gut hormone-based (e.g. GLP-1 receptor agonist or GLP-1-RA) pharmacotherapies which mimic the effect of bariatric surgery show impressive efficacy on weight reduction by modulation of food behaviour. However, the mechanisms of such functional changes, and how they relate to food decision-making and food purchase behaviour remain unknown. In Part 2 of the BrainFood-project, the investigators propose a novel approach using digital receipts from loyalty card to unravel the effect of obesity treatments (surgical and non-surgical) on eating and food purchase behaviour in daily life.
This study aims to compare, in subjects with obesity-hypoventilation syndrome (OHS) treated by long-term non-invasive ventilation (NIV), resting energy expenditure (REE) in spontaneous breathing and under NIV. The hypothesise of this study is that REE will be lower under NIV than under spontaneous breathing.
This study is exploring the association between vitamin D and Type 2 diabetes risk in normal weight and overweight UK adults.
The purpose of this study is to study the role of sympathetic mechanisms involved in chronic regulation of cardiovascular and metabolic abnormalities seen in obesity. The investigators will study the effects chronic sympathetic inhibition on insulin sensitivity, inflammation and endothelial function in obese hypertensive human subjects.
Inflammatory rheumatic diseases (IRD), such as rheumatoid arthritis, are characterized by adverse changes in body composition. Lean mass and bone mineral density are usually reduced while adiposity (total fat mass, visceral adiposity…) is increased in comparison with healthy controls. Many factors may influence the body composition of those patients such as aging, Disease Modifying Anti-Rheumatic Drugs (DMARDs), nutrition and physical activity. However, data on body composition and adverse changes under DMARDs in patients with rheumatoid arthritis (RA) are actually scarce. This is the case with tofacitinib (targeted synthetic DMARD or tsDMARD) while preliminary data let us think that this treatment may influence body composition and bone mineral density. This study is going to be the first to focus on changes in body composition (fat mass and lean mass), bone mineral density and bone marrow adiposity under tofacitinib.
Muscle insulin resistance is a hallmark of upper body obesity (UBO) and Type 2 diabetes (T2DM). It is unknown whether muscle free fatty acid (FFA) availability or intramyocellular fatty acid trafficking is responsible for the abnormal response to insulin. Likewise, the investigators do not understand to what extent the incorporation of FFA into ceramides or diacylglycerols (DG) affect insulin signaling and muscle glucose uptake. The investigators will measure muscle FFA storage into intramyocellular triglyceride, intramyocellular fatty acid trafficking, activation of the insulin signaling pathway and glucose disposal rates under both saline control (high overnight FFA) and after an overnight infusion of intravenous niacin (lower/normal FFA) to provide the first integrated examination of the interaction between FFA and muscle insulin action from the whole body to the cellular/molecular level. By identifying which steps in the insulin signaling pathway are most affected, the investigators will determine the site-specific effect of ceramides and/or DG on different degrees of insulin resistance. Hypothesis 1: Greater trafficking of plasma FFA into intramyocellular DG will impair proximal insulin signaling and reduce muscle glucose uptake. Hypothesis 2: Lowering FFA in UBO and T2DM by using an intravenous infusion of niacin will alter trafficking of plasma FFA into intramyocellular ceramides in a way that will improve insulin signaling and increase muscle glucose uptake. Hypothesis 3: Lowering FFA in UBO and T2DM by using an intravenous infusion of niacin will alter trafficking of plasma FFA into intramyocellular DG in a way that will improve insulin signaling and increase muscle glucose uptake.