PMID- 31972234
OWN - NLM
STAT- MEDLINE
DCOM- 20200814
LR  - 20200814
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Linking)
VI  - 432
DP  - 2020 Feb 28
TI  - Effects of prenatal nicotine exposure on hepatic glucose and lipid metabolism in 
      offspring rats and its hereditability.
PG  - 152378
LID - S0300-483X(20)30017-2 [pii]
LID - 10.1016/j.tox.2020.152378 [doi]
AB  - Prenatal nicotine exposure (PNE) could induce an increased susceptibility to 
      multiple chronic diseases in adult offspring, that mainly caused by intrauterine 
      maternal glucocorticoid (GC) over-exposure. We investigated the changes and 
      inheritability of hepatic glucose and lipid metabolism caused by PNE, to decipher 
      the possible intrauterine programming mechanism. Pregnant Wistar rats were 
      administered subcutaneously with 2 mg/kg.d nicotine from gestational day (GD) 
      9 approximately 20, and second-generation (F2) were set according to the mating between control 
      females and PNE males. The results showed that serum phenotypes and hepatic 
      enzymes of glucose and lipid metabolism were lower in F1 fetal rats of PNE but 
      higher in the F1 adult rats. Meanwhile, the activated states of hepatic 
      glucocorticoid-activation system, including type 1 and type 2 11beta-hydroxysteroid 
      dehydrogenases (Hsd11b1/2), nuclear receptor subfamily 3, group C, member 1 
      (Nr3c1) and CCAAT enhancer binding protein alpha (Cebpa), were positively correlated 
      with serum corticosterone levels but negatively correlated with the histone 
      acetylation (H3K27ac) and expression levels of insulin-like growth factor 1 
      (Igf1) before and after birth. Furthermore, serum phenotypes and hepatic enzymes 
      of glucose and lipid metabolism were lower in both F2 fetal and adult rats of 
      PNE, which were consistent with the hepatic changes of GC-IGF1 axis and the 
      glucocorticoid-activation system. In conclusion, PNE could lead to inheritable 
      changes of hepatic glucose and lipid metabolism, which are related to the 
      intrauterine programming of GC-IGF1 axis induced by the glucocorticoid-activation 
      system.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Hu, Wen
AU  - Hu W
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan, 430071, China.
FAU - Wang, Guihua
AU  - Wang G
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan, 430071, China.
FAU - He, Bo
AU  - He B
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan, 430071, China.
FAU - Hu, Shuwei
AU  - Hu S
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan, 430071, China.
FAU - Luo, Hanwen
AU  - Luo H
AD  - Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 
      430071, China.
FAU - Wen, Yinxian
AU  - Wen Y
AD  - Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 
      430071, China.
FAU - Chen, Liaobin
AU  - Chen L
AD  - Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 
      430071, China; Hubei Provincial Key Laboratory of Developmentally Originated 
      Disease, Wuhan, 430071, China.
FAU - Wang, Hui
AU  - Wang H
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan, 430071, China; Hubei Provincial Key Laboratory of Developmentally 
      Originated Disease, Wuhan, 430071, China. Electronic address: 
      wanghui19@whu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200120
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Glucocorticoids)
RN  - 0 (Insulin)
RN  - 0 (Nicotinic Agonists)
RN  - 0 (insulin-like growth factor-1, rat)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 6M3C89ZY6R (Nicotine)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Epigenesis, Genetic/drug effects
MH  - Female
MH  - Fetal Development
MH  - Gene Expression Regulation/drug effects
MH  - Glucocorticoids/metabolism
MH  - Glucose/*metabolism
MH  - Insulin/metabolism
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Lipid Metabolism/*drug effects/*genetics
MH  - Liver/*metabolism
MH  - Maternal Exposure
MH  - Nicotine/*toxicity
MH  - Nicotinic Agonists/*toxicity
MH  - Phenotype
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/genetics/*psychology
MH  - Rats
MH  - Rats, Wistar
OTO - NOTNLM
OT  - Epigenetic modification
OT  - Glucocorticoid
OT  - Glucose and lipid metabolism
OT  - Intrauterine programming of glucocorticoid-insulin-like growth factor 1 axis
OT  - Prenatal nicotine exposure
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/01/24 06:00
MHDA- 2020/08/15 06:00
CRDT- 2020/01/24 06:00
PHST- 2019/10/17 00:00 [received]
PHST- 2019/12/26 00:00 [revised]
PHST- 2020/01/18 00:00 [accepted]
PHST- 2020/01/24 06:00 [pubmed]
PHST- 2020/08/15 06:00 [medline]
PHST- 2020/01/24 06:00 [entrez]
AID - S0300-483X(20)30017-2 [pii]
AID - 10.1016/j.tox.2020.152378 [doi]
PST - ppublish
SO  - Toxicology. 2020 Feb 28;432:152378. doi: 10.1016/j.tox.2020.152378. Epub 2020 Jan 
      20.