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 journalArticle

12 Citations (Scopus)
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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.
Original languageEnglish
Pages (from-to)177-185
Number of pages9
JournalObesity Surgery
Volume27
Issue number1
Early online date30 Aug 2016
DOIs
Publication statusPublished - Jan 2017

Fingerprint

Hunger
Obesity
Eating
Body Weight
Hypothalamus
Receptor, Melanocortin, Type 4
Leptin Receptors
Equipment and Supplies
Glucagon-Like Peptide 1
Gastric Acid
Insulin Receptor
Gastrins
Brain
Laboratory Animals
Tyrosine 3-Monooxygenase
Transforming Growth Factors
Somatostatin
Glucagon
Interleukin-1
Brain Stem

Keywords

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

Cite this

Vagal Blocking for Obesity Control : a Possible Mechanism-Of-Action. / Johannessen, Helene; Revesz, David; Kodama, Yosuke; Cassie, Nikki; Skibicka, Karolina P.; Barrett, Perry; Dickson, Suzanne L.; Holst, Jens J.; Rehfeld, Jens F.; van der Plasse, Geoffrey; Adan, Roger A. H.; Kulseng, Bard; Ben-Menachem, Elinor; Chen, Duan.

In: Obesity Surgery, Vol. 27, No. 1, 01.2017, p. 177-185.

Research output: Contribution to journalArticle

Johannessen, H, Revesz, D, Kodama, Y, Cassie, N, Skibicka, KP, Barrett, P, Dickson, SL, Holst, JJ, Rehfeld, JF, van der Plasse, G, Adan, RAH, Kulseng, B, Ben-Menachem, E & Chen, D 2017, 'Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action', Obesity Surgery, vol. 27, no. 1, pp. 177-185. https://doi.org/10.1007/s11695-016-2278-x, https://doi.org/10.1007/s11695-016-2370-2
Johannessen, Helene ; Revesz, David ; Kodama, Yosuke ; Cassie, Nikki ; Skibicka, Karolina P. ; Barrett, Perry ; Dickson, Suzanne L. ; Holst, Jens J. ; Rehfeld, Jens F. ; van der Plasse, Geoffrey ; Adan, Roger A. H. ; Kulseng, Bard ; Ben-Menachem, Elinor ; Chen, Duan. / Vagal Blocking for Obesity Control : a Possible Mechanism-Of-Action. In: Obesity Surgery. 2017 ; Vol. 27, No. 1. pp. 177-185.
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title = "Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action",
abstract = "BackgroundRecently, the US FDA has approved “vagal blocking therapy or vBLoc{\circledR} 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.MethodsRats 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.ResultsVBLOC 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.ConclusionsBased on the present study, we may suggest that VBLOC induces satiety through vagal signaling, leading to reduced food intake and loss of body weight.",
keywords = "body weight, food intake, gut-brain axis, rats, vagus nerve",
author = "Helene Johannessen and David Revesz and Yosuke Kodama and Nikki Cassie and Skibicka, {Karolina P.} and Perry Barrett and Dickson, {Suzanne L.} and Holst, {Jens J.} and Rehfeld, {Jens F.} and {van der Plasse}, Geoffrey and Adan, {Roger A. H.} and Bard Kulseng and Elinor Ben-Menachem and Duan Chen",
note = "14 September 2016 Erratum to: Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action Helene Johannessen, David Revesz, Yosuke Kodama, Nikki Cassie, Karolina P Skibicka, Perry Barrett, Suzanne Dickson, Jens Holst, Jens Rehfeld, Geoffrey van der Plasse, Roger Adan, B{\aa}rd Kulseng, Elinor Ben-Menachem, Chun-Mei Zhao, Duan Chen, 2016, 2016. Obesity surgery. In the original article on page 4 the figures are referred to as (Fig. 1b-d) and (Fig. 1e) in the text. The correct reference is (Fig. 1b-e) and (Fig. 1f), respectively. In the original article on page 5 the figures are referred to as (Fig. 3c) and (Fig. 3d) in the text. The correct reference is (Fig. 3c,d) and (Fig. 3e,f), respectively. ",
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month = "1",
doi = "10.1007/s11695-016-2278-x",
language = "English",
volume = "27",
pages = "177--185",
journal = "Obesity Surgery",
issn = "0960-8923",
publisher = "Springer New York",
number = "1",

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T1 - Vagal Blocking for Obesity Control

T2 - a Possible Mechanism-Of-Action

AU - Johannessen, Helene

AU - Revesz, David

AU - Kodama, Yosuke

AU - Cassie, Nikki

AU - Skibicka, Karolina P.

AU - Barrett, Perry

AU - Dickson, Suzanne L.

AU - Holst, Jens J.

AU - Rehfeld, Jens F.

AU - van der Plasse, Geoffrey

AU - Adan, Roger A. H.

AU - Kulseng, Bard

AU - Ben-Menachem, Elinor

AU - Chen, Duan

N1 - 14 September 2016 Erratum to: Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action Helene Johannessen, David Revesz, Yosuke Kodama, Nikki Cassie, Karolina P Skibicka, Perry Barrett, Suzanne Dickson, Jens Holst, Jens Rehfeld, Geoffrey van der Plasse, Roger Adan, Bård Kulseng, Elinor Ben-Menachem, Chun-Mei Zhao, Duan Chen, 2016, 2016. Obesity surgery. In the original article on page 4 the figures are referred to as (Fig. 1b-d) and (Fig. 1e) in the text. The correct reference is (Fig. 1b-e) and (Fig. 1f), respectively. In the original article on page 5 the figures are referred to as (Fig. 3c) and (Fig. 3d) in the text. The correct reference is (Fig. 3c,d) and (Fig. 3e,f), respectively. 

PY - 2017/1

Y1 - 2017/1

N2 - BackgroundRecently, 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.MethodsRats 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.ResultsVBLOC 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.ConclusionsBased on the present study, we may suggest that VBLOC induces satiety through vagal signaling, leading to reduced food intake and loss of body weight.

AB - BackgroundRecently, 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.MethodsRats 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.ResultsVBLOC 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.ConclusionsBased on the present study, we may suggest that VBLOC induces satiety through vagal signaling, leading to reduced food intake and loss of body weight.

KW - body weight

KW - food intake

KW - gut-brain axis

KW - rats

KW - vagus nerve

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