View clinical trials related to Obesity, Abdominal.
Filter by:Study the effects of different exercise modes on total and regional adiposity variation in subcutaneous and visceral adipose tissue (VAT and SAT). The investigators hypothesize that total abdominal will improve for all the exercise groups compared to the control group. When comparing intervention groups: 1) no differences on the degree of improvement in total abdominal fat depots (VAT and SAT) 2) different degree of change when comparing specific sections at VAT and SAT are expected.
There is an ongoing and worsening problem with obesity in the developed, and much of the developing world. Although it has long been realized that Western diets that are rich in sugar and fat play an important role in this, it has only recently been realized that exposure to these diets, particularly in childhood, can damage the part of the brain that determines how much fat there is in the body. The result of this damage is that the so-called "set-point" for fat in this part of the brain is pushed upwards. There is a lot of evidence from animals that activating the brain's balance (vestibular) system pushes this set-point for fat downwards to cause fat loss, probably because this tricks the brain into thinking that the animal is more physically active. The aim of this study is to see whether the same effect can be triggered in humans by non-invasively stimulating the vestibular system with a small electrical current through the skin behind their ears.
This study will recruit 40 obese Hispanic youth (12 - 18 years of age who are greater than or equal to Tanner stage 4) from hospitals, clinics, and community centers. Participants will be randomly assigned to 16 weeks of probiotics (3 packets/day of VSL#3) or matched placebo. The purpose of this study is to demonstrate through a proof-of-concept trial that probiotics have the potential to alter the gut microbiome and gut hormones.
The prevalence of obesity and obesity-related complications is currently taking epidemic proportions. These complications increase the risk of type 2 diabetes and cardiovascular disease, which are important causes of morbidity and mortality worldwide. It is important to gain insight in the mechanisms underlying obesity-related complications, because this may lead to the development of directed therapeutic strategies. Currently, there is significant evidence that the cause of both insulin resistance and hypertension must be sought at the level of the microcirculation. Over activity of the renin-angiotensin-aldosterone system is a potential cause of microvascular dysfunction. Angiotensin II was indeed found to be implicated in the pathogenesis of obesity-associated hypertension and insulin resistance, possibly through interference with the vascular effects of insulin. Increased aldosterone levels have also been associated with resistant hypertension and insulin resistance, which is illustrated in patients with primary aldosteronism. Furthermore, aldosterone is known to exert several detrimental effects on the vasculature, some of which are offset by mineralocorticoid receptor antagonists. In obese individuals, plasma aldosterone concentrations are increased as well. We hypothesize that increased aldosterone levels in adipose persons induce microvascular dysfunction, which contributes to the development of insulin resistance and hypertension, and mineralocorticoid receptor antagonism results in improved insulin sensitivity and decreased blood pressure by counteracting the adverse effects of aldosterone on the microvasculature.
The main objective of this study is to evaluate efficacy and safety of ALS-L1023 tablet in patients with abdominal obesity of metabolic syndrome.
Part 1 determined: aliskiren, amlodipine and angiotensin II concentrations in interstitial fluid of fat and skeletal muscle; aliskiren and angiotensin II concentrations, and renin activity and concentration in fat and skeletal muscle tissues (biopsies); aliskiren, amlodipine and angiotensin II concentrations, and renin activity and concentration in plasma. Part 2 investigated the potential for aliskiren to modulate renin-angiotensin-aldosterone system (RAAS) activity, and lipid/carbohydrate metabolism in adipose and skeletal muscle tissue in obese patients with hypertension in comparison to amlodipine.