Abstract
Background
Nesfatin-1, a recently identified satiety molecule derived from nucleobindin 2 (NUCB2), is associated with visceral hypersensitivity in rats and is expressed in the amygdala. We tested the hypothesis that nesfatin-1 expression in the amygdala is involved in the pathogenesis of irritable bowel syndrome (IBS) visceral hypersensitivity.
Methods
An animal model of IBS-like visceral hypersensitivity was established using maternal separation (MS) during postnatal days 2–16. The role of nesfatin-1 in the amygdala on visceral sensitivity was evaluated.
Key Results
Rats subjected to MS showed a significantly increased mean abdominal withdrawal reflex (AWR) score and electromyographic (EMG) activity at 40, 60, and 80 mmHg colorectal distension. Plasma concentrations of nesfatin-1 and corticosterone were significantly higher than in non-handled (NH) rats. mRNA and protein expression of nesfatin-1/NUCB2 in the amygdala were increased in MS rats, but not in NH rats. In MS rats, AWR scores and EMG activity were significantly decreased after anti-nesfatin-1/NUCB2 injection. In normal rats, mean AWR score, EMG activity, and corticosterone expression were significantly increased after nesfatin-1 injection into the amygdala. Nesfatin-1-induced visceral hypersensitivity was abolished following application of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) antagonists.
Conclusions & Inferences
Elevated expression of nesfatin-1/NUCB2 in the amygdala in MS rats suggests a potential role in the pathogenesis of visceral hypersensitivity, which could potentially take place via activation of GR and MR signaling pathways.
This study provides novel evidence that nesfatin-1 in the amygdala may participate in the pathophysiology of IBS-like visceral hypersensitivity, which may be mediated, at least in part, by GR and MR signaling.
from Swallowing and Swallowing Disorders (Dysphagia) via a.lsfakia on Inoreader http://ift.tt/29NbEss
via IFTTT
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου