Prenatal caffeine exposure induced high susceptibility to metabolic syndrome in adult female offspring rats and its underlying mechanisms

被引：12
作者：
Pei, Lin-guo [1 ,3 ]
Yuan, Chao [1 ]
Guo, Yi-tian [1 ]
Kou, Hao [1 ,2 ]
Xia, Li-ping [1 ,2 ]
Zhang, Li [1 ]
Yan, You-e [1 ]
Xu, Dan [1 ,2 ]
Wang, Hui [1 ,2 ]
机构：
[1] Wuhan Univ, Basic Med Sch, Dept Pharmacol, Wuhan 430071, Peoples R China
[2] Hubei Prov Key Lab Dev Originated Dis, Wuhan, Peoples R China
[3] Nanyang Med Univ, Basic Med Coll, Nanyang 473061, Peoples R China
来源：
REPRODUCTIVE TOXICOLOGY | 2017年 / 71卷
基金：
中国国家自然科学基金;
关键词：
Prenatal caffeine exposure; Metabolic syndrome; Catch-up growth; Insulin resistance; CORONARY-HEART-DISEASE; FATTY LIVER-DISEASE; CHOLESTEROL RATIO; STEROIDOGENIC FACTOR-1; PROGRAMMING ALTERATION; INSULIN-RESISTANCE; EARLY NUTRITION; FETAL; GROWTH; MODEL;
D O I：
10.1016/j.reprotox.2017.06.045
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Our previous studies have demonstrated that prenatal caffeine exposure (PCE) induced an intrauterine programming of hypothalamic-pituitary-adrenal axis (HPAA)-associated neuroendocrine metabolism in 3-month-old offspring rats. In this study, we aimed to confirm this programming disorder and high susceptibility to metabolic syndrome (MS) in 10-month-old female PCE offspring with postnatal catch-up growth. We found that PCE female offspring rats showed decreased bodyweight but a higher rate of weight gain after birth. Moreover, in the offspring, basal hyperinsulinemia and insulin resistance were observed before unpredictable chronic stress (UCS), but serum total cholesterol (TCH) levels and triglyceride/high-density lipoprotein-cholesterol (TG/HDL-C), TCH/HDL-C and low-density lipoprotein-cholesterol/HDL-C (LDL-C/HDL-C) ratio changes were increased after UCS, accompanied by morphological damage of the related tissues. These results suggested that PCE adult female offspring rats were highly susceptible to MS, which is related to HPAA-associated neuroendocrine-metabolic programming disorder. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码：150 / 158
页数：9
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