Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action

Helene Johannessen, David Revesz, Yosuke Kodama, Nikki Cassie, Karolina P. Skibicka, Perry Barrett, Suzanne L. Dickson, Jens J. Holst, Jens F. Rehfeld, Geoffrey van der Plasse, Roger A. H. Adan, Bard Kulseng, Elinor Ben-Menachem, Duan Chen

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)
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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.

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.

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.

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.
Original languageEnglish
Pages (from-to)177-185
Number of pages9
JournalObesity Surgery
Issue number1
Early online date30 Aug 2016
Publication statusPublished - Jan 2017


  • body weight
  • food intake
  • gut-brain axis
  • rats
  • vagus nerve


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