Katharine F Hunt1, Joel T Dunn2, Carel W le Roux3, Laurence J Reed4, Paul K Marsden2, Ameet G Patel5, Stephanie A Amiel6. 1. Division of Diabetes and Nutritional Sciences, King's College London, London, U.K. King's College Hospital NHS Foundation Trust, London, U.K. katharine.f.hunt@kcl.ac.uk. 2. Division of Imaging Sciences and Biomedical Engineering, King's College London, London, U.K. 3. Diabetes Complications Research Centre, Conway Institute, University College Dublin, Dublin, Ireland Investigative Science, Imperial College London, London, U.K. 4. North Middlesex University Hospital, London, U.K. 5. King's College Hospital NHS Foundation Trust, London, U.K. 6. Division of Diabetes and Nutritional Sciences, King's College London, London, U.K. King's College Hospital NHS Foundation Trust, London, U.K.
Abstract
OBJECTIVE: Improved appetite control, possibly mediated by exaggerated gut peptide responses to eating, may contribute to weight loss after Roux-en-Y gastric bypass (RYGB). This study compared brain responses to food ingestion between post-RYGB (RYGB), normal weight (NW), and obese (Ob) unoperated subjects and explored the role of gut peptide responses in RYGB. RESEARCH DESIGN AND METHODS: Neuroimaging with [(18)F]-fluorodeoxyglucose (FDG) positron emission tomography was performed in 12 NW, 21 Ob, and 9 RYGB (18 ± 13 months postsurgery) subjects after an overnight fast, once FED (400 kcal mixed meal), and once FASTED, in random order. RYGB subjects repeated the studies with somatostatin infusion and basal insulin replacement. Fullness, sickness, and postscan ad libitum meal consumption were measured. Regional brain FDG uptake was compared using statistical parametric mapping. RESULTS: RYGB subjects had higher overall fullness and food-induced sickness and lower ad libitum consumption. Brain responses to eating differed in the hypothalamus and pituitary (exaggerated activation in RYGB), left medial orbital cortex (OC) (activation in RYGB, deactivation in NW), right dorsolateral frontal cortex (deactivation in RYGB and NW, absent in Ob), and regions mapping to the default mode network (exaggerated deactivation in RYGB). Somatostatin in RYGB reduced postprandial gut peptide responses, sickness, and medial OC activation. CONCLUSIONS: RYGB induces weight loss by augmenting normal brain responses to eating in energy balance regions, restoring lost inhibitory control, and altering hedonic responses. Altered postprandial gut peptide responses primarily mediate changes in food-induced sickness and OC responses, likely to associate with food avoidance.
OBJECTIVE: Improved appetite control, possibly mediated by exaggerated gut peptide responses to eating, may contribute to weight loss after Roux-en-Y gastric bypass (RYGB). This study compared brain responses to food ingestion between post-RYGB (RYGB), normal weight (NW), and obese (Ob) unoperated subjects and explored the role of gut peptide responses in RYGB. RESEARCH DESIGN AND METHODS: Neuroimaging with [(18)F]-fluorodeoxyglucose (FDG) positron emission tomography was performed in 12 NW, 21 Ob, and 9 RYGB (18 ± 13 months postsurgery) subjects after an overnight fast, once FED (400 kcal mixed meal), and once FASTED, in random order. RYGB subjects repeated the studies with somatostatin infusion and basal insulin replacement. Fullness, sickness, and postscan ad libitum meal consumption were measured. Regional brain FDG uptake was compared using statistical parametric mapping. RESULTS: RYGB subjects had higher overall fullness and food-induced sickness and lower ad libitum consumption. Brain responses to eating differed in the hypothalamus and pituitary (exaggerated activation in RYGB), left medial orbital cortex (OC) (activation in RYGB, deactivation in NW), right dorsolateral frontal cortex (deactivation in RYGB and NW, absent in Ob), and regions mapping to the default mode network (exaggerated deactivation in RYGB). Somatostatin in RYGB reduced postprandial gut peptide responses, sickness, and medial OC activation. CONCLUSIONS: RYGB induces weight loss by augmenting normal brain responses to eating in energy balance regions, restoring lost inhibitory control, and altering hedonic responses. Altered postprandial gut peptide responses primarily mediate changes in food-induced sickness and OC responses, likely to associate with food avoidance.
Authors: Mohammed K Hankir; Michael Rullmann; Florian Seyfried; Sven Preusser; Sindy Poppitz; Stefanie Heba; Konstantinos Gousias; Jana Hoyer; Tatjana Schütz; Arne Dietrich; Karsten Müller; Burkhard Pleger Journal: JCI Insight Date: 2019-10-03
Authors: Anna Aulinas; Reitumetse L Pulumo; Elisa Asanza; Christopher J Mancuso; Meghan Slattery; Christiane Tolley; Franziska Plessow; Jennifer J Thomas; Kamryn T Eddy; Karen K Miller; Anne Klibanski; Madhusmita Misra; Elizabeth A Lawson Journal: J Clin Endocrinol Metab Date: 2019-04-01 Impact factor: 5.958
Authors: Anna Aulinas; Franziska Plessow; Reitumetse L Pulumo; Elisa Asanza; Christopher J Mancuso; Meghan Slattery; Christiane Tolley; Jennifer J Thomas; Kamryn T Eddy; Karen K Miller; Anne Klibanski; Madhusmita Misra; Elizabeth A Lawson Journal: J Clin Endocrinol Metab Date: 2019-10-01 Impact factor: 5.958
Authors: Robyn M Brown; Eva Guerrero-Hreins; Wendy A Brown; Carel W le Roux; Priya Sumithran Journal: Nat Rev Endocrinol Date: 2021-07-14 Impact factor: 43.330