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Biomed Res Int. 2016;2016:5251738. doi: 10.1155/2016/5251738. Epub 2016 Jun 29.

Progressive Depletion of Rough Endoplasmic Reticulum in Epithelial Cells of the Small Intestine in Monosodium Glutamate Mice Model of Obesity.

Author information

1
Department of Basic Science, Educational and Research Center for Pharmacy, Meiji Pharmaceutical University, Tokyo 204-8588, Japan.
2
Faculty of Pharmaceutical Sciences, Meiji Pharmaceutical University, Tokyo 204-8588, Japan.
3
Department of Pharmacology and Toxicology, Dokkyo Medical University School of Medicine, Tochigi 321-0293, Japan.

Abstract

Chronic obesity is a known risk factor for metabolic syndrome. However, little is known about pathological changes in the small intestine associated with chronic obesity. This study investigated cellular and subcellular level changes in the small intestine of obese mice. In this study, a mouse model of obesity was established by early postnatal administration of monosodium glutamate. Changes in body weight were monitored, and pathological changes in the small intestine were evaluated using hematoxylin-eosin and Nissl staining and light and electron microscopy. Consequently, obese mice were significantly heavier compared with controls from 9 weeks of age. Villi in the small intestine of obese mice were elongated and thinned. There was reduced hematoxylin staining in the epithelium of the small intestine of obese mice. Electron microscopy revealed a significant decrease in and shortening of rough endoplasmic reticulum in epithelial cells of the small intestine of obese mice compared with normal mice. The decrease in rough endoplasmic reticulum in the small intestine epithelial cells of obese mice indicates that obesity starting in childhood influences various functions of the small intestine, such as protein synthesis, and could impair both the defense mechanism against invasion of pathogenic microbes and nutritional absorption.

PMID:
27437400
PMCID:
PMC4942597
DOI:
10.1155/2016/5251738
[Indexed for MEDLINE]
Free PMC Article

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