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    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Current Opinion in Endocrinology, Diabetes & Obesity Vol. 25, No. 1 ( 2018-02), p. 3-11
    In: Current Opinion in Endocrinology, Diabetes & Obesity, Ovid Technologies (Wolters Kluwer Health), Vol. 25, No. 1 ( 2018-02), p. 3-11
    Kurzfassung: Reduced energy intake, resulting from favourable changes in eating behaviour, is the predominant driver of weight loss following bariatric surgery. Here we review the most recent studies examining the impact of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy, the two most common bariatric procedures, upon eating behaviour and the suggested underlying biological mechanisms. Recent findings Following RYGB or sleeve gastrectomy, most people report subjective changes in appetite, taste and food preference, with decreased high-fat preference most commonly reported. Objective postsurgery changes in taste and olfactory acuity occur. A new phenomenon, ‘meal-size aversion’, may contribute to reduced postoperative energy intake. Recent studies provide evidence for peptide YY3–36, glucagon-like peptide-1, ghrelin, neurotensin and oleoylethanolamide as mediators of postoperative eating behaviour changes. Factors modulating these changes include sex, type 2 diabetes status, genetics and bariatric procedure. New studies implicate central dopaminergic and opioid receptor signalling as key neural mediators driving altered eating behaviour. Brain neuroimaging studies show that obesity-associated changes in food-cue responses, brain connectivity and structural abnormalities are normalized following bariatric surgery. Summary Understanding the biological mechanisms mediating the eating behaviour changes engendered by bariatric surgery may lead to the development of novel therapeutic strategies for people with obesity.
    Materialart: Online-Ressource
    ISSN: 1752-296X , 1752-2978
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2018
    ZDB Id: 2273420-X
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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