View clinical trials related to Appetite Control.
Filter by:Disturbances in brain insulin-sensitivity are not only observed in obesity and type 2 diabetes (T2D), but also during brain aging and in dementia. Ketone monoester supplements may improve brain insulin-sensitivity, which can be quantified by measuring the gray-matter cerebral blood flow (CBF) response to intranasally administered insulin. We hypothesize that acute ketone monoester supplementation increases (regional) brain vascular function and insulin-sensitivity thereby improving cognitive performance and appetite control. The primary objective is to evaluate in older men the acute effect of ketone monoester supplementation on (regional) brain vascular function and insulin-sensitivity, as quantified by the non-invasive gold standard magnetic resonance imaging (MRI)-perfusion method Arterial Spin Labelling (ASL). The CBF response to intranasal insulin is a robust and sensitive physiological marker of brain insulin-sensitivity. Secondary objectives are to investigate effects on cognitive performance as assessed with a neuropsychological test battery, and appetite control as quantified by functional MRI (fMRI) with visual food cues.
The management of body mass and energy balance requires a better understanding and mastery of the interactions between our daily activities, such as physical exercise, and the control of our food intake. Over the past 15 years, many studies have focused on the potential effects of physical exercise on this satiety cascade and on subsequent food intake, in many populations. Thus, both in normal-weight subjects and in patients suffering from overweight and obesity, it has been shown that the performance of an acute exercise of moderate intensity promotes a transient anorectic effect, reducing feelings of hunger post -exercise, and can even induce a reduction in subsequent food intake. In healthy young adults, recent results show that high-intensity physical exercise can reduce feelings of hunger and increase the satietogenic effect of a meal compared to a control condition and low-intensity exercise. intensity. Nevertheless, it seems that the food reward (which refers to the notion of food reward) does not respond in the same way, the authors not observing any change in either liking or wanting, regardless of exercise intensity. Importantly, this literature uses ad libitum test meals, wishing to assess both satietogenic, hedonic and purely nutritional responses (assessing the amount of food intake). Nevertheless, these sensory and hedonic responses to food intake have recently been shown to be sensitive to the composition of the meal and its caloric quantity, which could induce a significant bias as to the conclusions on the effects of physical exercise. Indeed, the use of meals ad libitum, by definition, leads to caloric intake and different meal compositions. Thus, it is possible that the results obtained are strongly impacted by the nature of the test meal more than by the exercise itself. It therefore remains uncertain today to conclude as to the effects of physical exercise on the factors of the satietogenic cascade, since beyond physical exercise, the test meals compared are not identical. It therefore seems important today to develop a more coherent and adapted methodology, to better study the food and satietogenic responses to our daily activities. In this context, the present project aims to compare the satietogenic response to a meal following acute exercise according to the nature of this meal (ad libitum versus calibrated) in healthy adults.