Helene Johannessen1, David Revesz2, Yosuke Kodama1, Nikki Cassie3, Karolina P Skibicka4, Perry Barrett3, Suzanne Dickson4, Jens Holst5, Jens Rehfeld6, Geoffrey van der Plasse7, Roger Adan7, Bård Kulseng8, Elinor Ben-Menachem2, Chun-Mei Zhao1, Duan Chen9. 1. Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway. 2. Department of Clinical Neuroscience and Rehabilitation, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden. 3. Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, Scotland. 4. Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. 5. Department of Biomedical Sciences, the Panum Institute, University of Copenhagen, Copenhagen, Denmark. 6. Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark. 7. Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, Netherlands. 8. Center for Obesity Research, Department of Surgery, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. 9. Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway. duan.chen@ntnu.no.
Abstract
BACKGROUND: Recently, the US FDA has approved "vagal blocking therapy or vBLoc® therapy" as a new treatment for obesity. The aim of the present study was to study the mechanism-of-action of "VBLOC" in rat models. METHODS: Rats were implanted with VBLOC, an intra-abdominal electrical device with leads placed around gastric vagal trunks through an abdominal incision and controlled by wireless device. Body weight, food intake, hunger/satiety, and metabolic parameters were monitored by a comprehensive laboratory animal monitoring system. Brain-gut responses were analyzed physiologically. RESULTS: VBLOC reduced body weight and food intake, which was associated with increased satiety but not with decreased hunger. Brain activities in response to VBLOC included increased gene expression of leptin and CCKb receptors, interleukin-1β, tumor necrosis factor, and transforming growth factor β1 in the brainstem; increased CCK, somatostatin, and tyrosine hydroxylase in the hippocampus; increased NPY, AgRP, and Foxa2 in the hypothalamus; and reduced CCKb receptor, melanocortin 4 receptor, and insulin receptor in the hypothalamus. Plasma concentrations of CCK, gastrin, glucagon, GLP-1, and PYY and gastric acid secretion were unchanged in response to VBLOC. CONCLUSIONS: Based on the present study, we may suggest that VBLOC induces satiety through vagal signaling, leading to reduced food intake and loss of body weight.
BACKGROUND: Recently, the US FDA has approved "vagal blocking therapy or vBLoc® therapy" as a new treatment for obesity. The aim of the present study was to study the mechanism-of-action of "VBLOC" in rat models. METHODS:Rats were implanted with VBLOC, an intra-abdominal electrical device with leads placed around gastric vagal trunks through an abdominal incision and controlled by wireless device. Body weight, food intake, hunger/satiety, and metabolic parameters were monitored by a comprehensive laboratory animal monitoring system. Brain-gut responses were analyzed physiologically. RESULTS: VBLOC reduced body weight and food intake, which was associated with increased satiety but not with decreased hunger. Brain activities in response to VBLOC included increased gene expression of leptin and CCKb receptors, interleukin-1β, tumornecrosis factor, and transforming growth factor β1 in the brainstem; increased CCK, somatostatin, and tyrosine hydroxylase in the hippocampus; increased NPY, AgRP, and Foxa2 in the hypothalamus; and reduced CCKb receptor, melanocortin 4 receptor, and insulin receptor in the hypothalamus. Plasma concentrations of CCK, gastrin, glucagon, GLP-1, and PYY and gastric acid secretion were unchanged in response to VBLOC. CONCLUSIONS: Based on the present study, we may suggest that VBLOC induces satiety through vagal signaling, leading to reduced food intake and loss of body weight.
Entities:
Keywords:
Body weight; Food intake; Gut-brain axis; Rats; Vagus nerve
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