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<h4 style="font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif;">OBJECTIVE:</h4><p style="margin: 0px 0px 0.5em; line-height: 1.538em; font-size: 1.04em; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">Improved appetite control, possibly mediated by exaggerated gut peptide responses to eating, may contribute to weight loss after Roux-en-Y&nbsp;<span class="highlight">gastric bypass</span>&nbsp;(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.</span></p><h4 style="font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">RESEARCH DESIGN AND METHODS:</span></h4><p style="margin: 0px 0px 0.5em; line-height: 1.538em; font-size: 1.04em; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">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.</span></p><h4 style="font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">RESULTS:</span></h4><p style="margin: 0px 0px 0.5em; line-height: 1.538em; font-size: 1.04em; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">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.</span></p><h4 style="font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">CONCLUSIONS:</span></h4><p style="margin: 0px 0px 0.5em; line-height: 1.538em; font-size: 1.04em; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 10pt;">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.</span></p> |