Search

We read with interest the study by Higuchi et al , which identified mechanisms of increased satiation in Cyp8b1−/− mice via slowed gastric empting.1 Following data showing that deleting Cyp8b1, which is required to produce 12α-hydroxylated bile acids, impaired intestinal lipid absorption in mice, the authors convincingly demonstrated that lowering 12α-hydroxylated bile acids slowed gastric emptying in Cyp8b1−/− mice.1 Duodenal lipid infusion affects gastric function, and duodenal hypersensitivity to lipids has been studied in GI disorders with gastric dysmotility, such as functional dyspepsia (FD).2 FD is defined by upper GI symptoms originating from the gastroduodenal region with no structural disease on routine investigation.3 Although studies showed that lipids are a major trigger of dyspeptic symptoms, the effect was only partially explained by duodenal release of cholecystokinin.4 Interestingly, the release of bile salts has been linked to the generation of dyspeptic symptoms, possibly via duodenal luminal or mucosal changes including hyperpermeability.5 6 However, duodenal alterations have not …