期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 44, 期 2, 页码 657-670出版社
KARGER
DOI: 10.1159/000485277
关键词
Hypercholesterolemia; Prenatal ethanol exposure; High-fat diet; Gender; Interaction; Intrauterine growth retardation
资金
- National Key Research and Development Program of China [2017YFC1001300]
- National Natural Science Foundation of China [81220108026, 81430089, 81673524]
- Hubei Province Health and Family Planning Scientific Research Project [WJ2017C0003]
Background/Aims: Prenatal ethanol exposure (PEE) could induce intrauterine programming of hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolism, resulting in intrauterine growth retardation and susceptibility to adult hypercholesterolemia in offspring. This study aimed to analyse the effects and interactions of PEE, a post-weaning high-fat diet (HFD) and gender on the occurrence of adult hypercholesterolemia in offspring rats. Methods: Wistar female rats were treated with ethanol (4 g/kg. d) at gestational days 11-20. The offspring were given a normal diet or HFD after weaning, and the blood cholesterol metabolism phenotype and expression of hepatic cholesterol metabolism related genes were detected in 24-week-old offspring. Furthermore, the interactions among PEE, HFD, and gender on hypercholesterolemia occurrence were analysed. Results: PEE increased the serum total cholesterol (TCH) and low-density lipoprotein-cholesterol (LDL-C) levels and decreased the serum high-density lipoprotein-cholesterol (HDL-C) level in adult offspring rats; the changes in female offspring were greater than those in males. At the same time, the mRNA expression levels of hepatic cholesterol metabolic enzymes (apolipoprotein B (ApoB) and 7 alpha-hydroxylase (CYP7A1))-were increased, while the mRNA expression levels of the scavenger receptor B1 (SR-B1) and LDL receptor (LDLR) were decreased. Furthermore, a three-way ANOVA showed there were interactions among PEE, post-weaning HFD and gender. For PEE offspring, a post-weaning HFD aggravated the elevated hepatic ApoB and CYP7A1 expression and reduced SR-B1 and LDLR expression; the changes in hepatic SR-B1 and CYP7A1 expression were greater in female HFD rats than in males. Conclusion: Our findings suggest that a post-weaning HFD could aggravate offspring hypercholesterolemia caused by PEE and that this mechanism might be associated with hepatic cholesterol metabolic disorders that are aggravated by a post- weaning HFD; hepatic cholesterol metabolism was more sensitive to neuroendocrine metabolic alterations by PEE and a post-weaning HFD in the female offspring than in the male offspring. (C) 2017 The Author(s) Published by S. Karger AG, Basel
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