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

Johannessen, H. (author)
Revesz, David (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Kodama, Y. (author)
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Cassie, N. (author)
Skibicka, Karolina P (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Barrett, P. (author)
Dickson, Suzanne L., 1966 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Holst, J. (author)
Rehfeld, J. (author)
van der Plasse, G. (author)
Adan, R. (author)
Kulseng, B. (author)
Ben-Menachem, Elinor, 1945 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Zhao, C. M. (author)
Chen, D. (author)
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 (creator_code:org_t)
2016-08-30
2017
English.
In: Obesity Surgery. - : Springer Science and Business Media LLC. - 0960-8923 .- 1708-0428. ; 27:1, s. 177-185
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kirurgi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Surgery (hsv//eng)

Keyword

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

Publication and Content Type

ref (subject category)
art (subject category)

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