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

doi:10.1007/s11695-016-2278-x

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

Institut for Klinisk Medicin

17 Citationer (Scopus)

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.

Originalsprog	Engelsk
Tidsskrift	Obesity Surgery
Vol/bind	27
Udgave nummer	1
Sider (fra-til)	177-185
Antal sider	9
ISSN	0960-8923
DOI	https://doi.org/10.1007/s11695-016-2278-x https://doi.org/10.1007/s11695-016-2370-2
Status	Udgivet - jan. 2017

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Johannessen, H., Revesz, D., Kodama, Y., Cassie, N., Skibicka, K. P., Barrett, P., Dickson, S., Holst, J., Rehfeld, J., van der Plasse, G., Adan, R., Kulseng, B., Ben-Menachem, E., Zhao, C.-M., & Chen, D. (2017). Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action. Obesity Surgery, 27(1), 177-185. https://doi.org/10.1007/s11695-016-2278-x, https://doi.org/10.1007/s11695-016-2370-2

Johannessen, H, Revesz, D, Kodama, Y, Cassie, N, Skibicka, KP, Barrett, P, Dickson, S, Holst, J , Rehfeld, J, van der Plasse, G, Adan, R, Kulseng, B, Ben-Menachem, E, Zhao, C-M & Chen, D 2017, 'Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action', Obesity Surgery, bind 27, nr. 1, s. 177-185. https://doi.org/10.1007/s11695-016-2278-x, https://doi.org/10.1007/s11695-016-2370-2

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abstract = "BACKGROUND: Recently, the US FDA has approved {"}vagal blocking therapy or vBLoc{\textregistered} 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.",

author = "Helene Johannessen and David Revesz and Yosuke Kodama and Nikki Cassie and Skibicka, {Karolina P} and Perry Barrett and Suzanne Dickson and Jens Holst and Jens Rehfeld and {van der Plasse}, Geoffrey and Roger Adan and B{\aa}rd Kulseng and Elinor Ben-Menachem and Chun-Mei Zhao and Duan Chen",

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doi = "10.1007/s11695-016-2278-x",

language = "English",

volume = "27",

pages = "177--185",

journal = "Obesity Surgery",

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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

AU - Holst, Jens

AU - Rehfeld, Jens

AU - van der Plasse, Geoffrey

AU - Adan, Roger

AU - Kulseng, Bård

AU - Ben-Menachem, Elinor

AU - Zhao, Chun-Mei

AU - Chen, Duan

PY - 2017/1

Y1 - 2017/1

N2 - 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.

AB - 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.

U2 - 10.1007/s11695-016-2278-x

DO - 10.1007/s11695-016-2278-x

M3 - Journal article

C2 - 27576578

SN - 0960-8923

VL - 27

SP - 177

EP - 185

JO - Obesity Surgery

JF - Obesity Surgery

IS - 1

ER -

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

Abstract

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