title: Prenatal nicotine exposure induced a hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolic programmed alteration in intrauterine growth retardation offspring rats.
abstract: 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 2mg/kgd 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.
authors.affiliation: Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 430071, China.
authors.forename: L
authors.initials: L
authors.lastname: Liu
authors.forename: F
authors.initials: F
authors.lastname: Liu
authors.forename: H
authors.initials: H
authors.lastname: Kou
authors.forename: B J
authors.initials: BJ
authors.lastname: Zhang
authors.forename: D
authors.initials: D
authors.lastname: Xu
authors.forename: B
authors.initials: B
authors.lastname: Chen
authors.forename: L B
authors.initials: LB
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Magdalou
authors.forename: H
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D005260:Female; D047109:Fetal Development / Q000187:drug effects / Q000502:physiology; D005317:Fetal Growth Retardation / Q000139:chemically induced* / Q000378:metabolism; D005731:Ganglionic Stimulants / Q000633:toxicity*; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000196:embryology / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D050356:Lipid Metabolism; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D008431:Maternal-Fetal Exchange; D009489:Neurosecretion / Q000187:drug effects*; D009538:Nicotine / Q000633:toxicity*; D010805:Physical Conditioning, Animal; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000187:drug effects / Q000502:physiology; D013550:Swimming
chemical_list: D005731:Ganglionic Stimulants; D009538:Nicotine; D005947:Glucose