Postnatal high-fat diet leads to spatial deficit, obesity, and central and peripheral inflammation in prenatal dexamethasone adult offspring rats

Chih Sung Hsieh, Shih Wen Li, Jiunn Ming Sheen, Hong Ren Yu, Mao Meng Tiao, You Lin Tain, Chung Hao Su, Li Tung Huang*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

4 引文 斯高帕斯(Scopus)

摘要

Synthetic glucocorticoids are frequently used in clinical practice for treating pregnant women at risk of preterm delivery, but their long-term effects on the infant brain are largely unknown. Pregnant Sprague-Dawley rats were administered vehicle or dexamethasone between gestational days 14 and 21. Male offspring were then weaned onto either a standard chow or a high-fat diet. The postnatal levels of insulin-like growth factor I (IGF-1), tumor necrosis factor-α (TNF-α), and asymmetric dimethylarginine (ADMA) in the plasma, liver, and brain were examined, as well as the possible effects of prenatal dexamethasone on cognition. We found that a postnatal high-fat diet led to spatial deficits detected by the Morris water maze in adult offspring administered dexamethasone prenatally. The spatial deficit was accompanied by decreased IGF-1 mRNA and increased ADMA levels in the dorsal hippocampus. In peripheral systems, a postnatal high-fat diet resulted in decreased plasma IGF-1, increased plasma corticosterone, increased concentrations of transaminases, TNF-α mRNA, and ADMA in the liver, and associated obesity in adult offspring administered prenatal dexamethasone. In conclusion, a postnatal high-fat diet led to spatial deficits, obesity, and altered levels of IGF-1, TNF-α, and ADMA in the plasma, liver, or brain.

原文英語
頁(從 - 到)818-825
頁數8
期刊NeuroReport
27
發行號11
DOIs
出版狀態已出版 - 01 08 2016

文獻附註

Publisher Copyright:
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

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