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

Artikel i vetenskaplig tidskrift
Författare H. Johannessen
David Revesz
Y. Kodama
N. Cassie
Karolina P Skibicka
P. Barrett
Suzanne L. Dickson
J. Holst
J. Rehfeld
G. van der Plasse
R. Adan
B. Kulseng
Elinor Ben-Menachem
C. M. Zhao
D. Chen
Publicerad i Obesity Surgery
Volym 27
Nummer/häfte 1
Sidor 177-185
ISSN 0960-8923
Publiceringsår 2017
Publicerad vid Institutionen för neurovetenskap och fysiologi
Sidor 177-185
Språk en
Länkar 10.1007/s11695-016-2278-x
Ämnesord Body weight, Food intake, Gut-brain axis, Rats, Vagus nerve, vagus nerve-stimulation, food-intake, body-weight, feeding-behavior, rats, hippocampus, surgery, mice, receptor, acid, Surgery, rloni g, 1986, physiology & behavior, v38, p321, BAS HT, 1994, YALE JOURNAL OF BIOLOGY AND MEDICINELester Dragstedt Centenary Symposium
Ämneskategorier Kirurgi

Sammanfattning

Recently, the US FDA has approved "vagal blocking therapy or vBLocA (R) 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-1 beta, tumor necrosis factor, and transforming growth factor beta 1 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.

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