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Vagal activation inhibits insulin release through neuronal nitric oxide synthase in obese male mice

delete2026-05-26
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PRE
AI
E
Emi Hashiuchi
Y
Y. Inaba
H
Hikaru Sugimoto
K
Kumi Kimura
H
Hitoshi Watanabe
M
Mayu Kajino
S
Shun‐ichiro Asahara
M
Masaki Kobayashi
O
Osamu Kikuchi
Y
Yoshitaka Hayashi
S
Shin‐ichi Horike
T
Takiko Daikoku
M
Michihiro Mieda
T
Takeshi Sakurai
M
Mashito Sakai
M
Michihiro Matsumoto
T
Tadahiro Kitamura
M
Makoto Sato
K
Kim Ravnskjær
M
Masato Kasuga
M
Mamoru Tanida
S
Shinya Kuroda
H
Hiroshi Inoue *
DOI:10.1126/scisignal.adz8805delete
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Abstract

Abstract

En 中文
Eating induces the release of insulin from the pancreas through cholinergic signaling mediated by vagal innervation of the pancreas. Using mice in which the activity of the vagal nerve could be manipulated, Hashiuchi et al. determined how insulin release was affected by obesity. Activation of the vagus nerve not only increased but also decreased plasma insulin concentrations, an effect that was partially revealed through mathematical modeling. Obesity exacerbated the insulin-decreasing effect of vagal activation, which was mediated through nitric oxide (NO) signaling and was reversed by vagal deletion of an NO-producing enzyme. These results show a more complex effect of vagal activity on insulin release than previously appreciated. —Wei Wong
Keywords:
vagal activation
insulin release
obesity
nitric oxide
neuronal nitric oxide synthase

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Science Signaling cover
Science Signaling
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