期刊
TOXICOLOGY LETTERS
卷 214, 期 3, 页码 307-313出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2012.09.001
关键词
Nicotine; Intrauterine growth retardation; Glucocorticoid; Hypothalamic-pituitary-adrenal axis; Glucose and lipid metabolism
类别
资金
- National Natural Science Foundation of China [30830112, 81072709, 81220108026]
- Key Grant of Chinese Ministry of Education [V200801]
- Hubei Province Science Foundation for Innovation Group [2009CDA079]
- [2001CDA042]
Prenatal nicotine exposure inhibits the functional development of the hypothalamic-pituitary-adrenal (HPA) axis and alters glucose and lipid metabolism in intrauterine growth retardation (IUGR) fetal rats, but the postnatal consequence is unknown. We aimed to verify a neuroendocrine metabolic programmed alteration in IUGR offspring whose mothers were subcutaneously treated with 2 mg/kg d of nicotine from gestational day 11 to 20. In the nicotine group, blood adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels were higher before postnatal day 35 and then returned to lower than the respective control. The adult offspring showed unchanged blood glucose but increased blood total cholesterol (TCH) and triglyceride (TG) levels. However, after chronic stress, the mRNA expression levels of hippocampal glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) were lower, but gain rates of ACTH and CORT levels were greater compared to the control. Additionally, the level of blood glucose was increased, while the elevated levels of blood TCH and TG before stress were close to the control levels. These results suggested that prenatal nicotine exposure induced an HPA axis-associated neuroendocrine metabolic programmed alteration in adult offspring, which might be attributed to hippocampal functional injury in utero. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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