For more information please contact Prof. dr. Roman Vangoitsenhoven, tel.: +32 16 34 47 55, mail: firstname.lastname@example.org or Mrs. Nathalie Weltens, tel.: +32 16 37 74 86, mail: email@example.com.You can apply for this job no later than June 30, 2021.
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For the current project, the laboratory for Clinical and Experimental Endocrinology (CEE) and the Laboratory for Brain-Gut Axis Studies (LaBGAS) have joined forces to further elucidate how the regulation of food intake changes after bariatric surgery. Both labs are situated at KU Leuven, Belgium – a top-ranked university in the heart of Europe (30 min to Brussels, 2 hours to London, Paris and Amsterdam)
The CEE-team of Bart Van der Schueren and Roman Vangoitsenhoven has an extensive track record in clinical and translational research focused on the metabolic consequences and side effects of bariatric surgery. The LaBGAS-team of Lukas Van Oudenhove and Nathalie Weltens has established an innovative research line that integrates biochemical techniques to study neurohumoral gut-brain signaling mechanisms with advanced neuroimaging techniques (including fMRI, radioligand PET and combined PET/MR imaging) to unravel how gastrointestinal hormones, nutrients and microbiota-related signals impact on cognitive and affective processes and their neurochemical basis. Funding for this project is available through internal (start-up grant for RVG, Methusalem for LVO) and external sources (FWO for NW).
Calorie-dense foods induce a positive reward signal in the brain. Dopamine is an essential neurotransmitter for reward signaling, motivation and execution of goal-directed behaviors. Studies have reported a decreased expression of dopamine D2 receptors in the brain of patients with obesity (Wang et al., 2001), whereas those receptors are upregulated after bariatric surgery (van der Zwaal et al.,2016). Intriguingly, dopamine also has peripheral effects on the gut and the pancreas such as inhibition of insulin secretion which could influence the development of type 2 diabetes (T2D), one of the major comorbidities of obesity. The relationship between central dopamine signaling and development of T2D, however, has not been assessed until now. In addition, the endocannabinoid system (ECS) has also emerged as a key regulator of food intake. ECS compounds are strategically localized at every level of the brain-gut axisto exert an energy-stowing function. In the brain, both endocannabinoids and their receptor (CB1R) are localized in homeostatic and reward regions, where they act as presynaptic modulator of neurotransmitter release, including dopamine. The LaBGAS group previously showed that CB1R availability in homeostatic and reward areas is differently linked to body mass index (BMI) in healthy subjects versus patients with various food intake disorders, including obesity (Weltens etal., 2016). It remains unknown, however, whether changes in CB1R availability area predisposing factor for, or the consequence of, aberrant BMI, and what the underlying gut-brain mechanisms are of this CB1R – BMI relationship. Specifically, differences in CB1R availability have never been linked to circulating endocannabinoid levels, although it is believed that the decreased central CB1R expression in obesity results from an overactive ECS. Further, as endocannabinoids are thought to actin tandem with metabolic hormones regulating hunger and satiety, the interplay between these hormone levels and the changes in cerebral CB1R availability should also be investigated. The major aim of the present PhD project is to study the role of endocannabinoid and dopamine signaling in relation to metabolic health before and after weight loss, by identifying the neurochemical and hormonal gut-brain signaling mechanisms underlying the changes in body weight and eating behaviour after bariatric surgery.
Thistranslates into 3 research objectives: