PMID- 24723259
OWN - NLM
STAT- MEDLINE
DCOM- 20150624
LR  - 20211021
IS  - 1559-0100 (Electronic)
IS  - 1355-008X (Linking)
VI  - 47
IP  - 2
DP  - 2014 Nov
TI  - Dioxin-induced fetal growth retardation: the role of a preceding attenuation in 
      the circulating level of glucocorticoid.
PG  - 572-80
LID - 10.1007/s12020-014-0257-3 [doi]
AB  - Exposure of pregnant rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at a low 
      dose causes developmental disorders such as growth retardation and sexual 
      immaturity in their pups. Our previous studies have demonstrated that TCDD 
      attenuates the expression of pituitary luteinizing hormone in fetuses, resulting 
      in the impairment of sexual behavior after they reach maturity. In this study, we 
      focused on growth disturbance and investigated whether TCDD affects the 
      expression of growth hormone (GH), another pituitary hormone which is essential 
      for normal development in perinatal pups. The result showed that maternal 
      exposure to TCDD (1 microg/kg) at gestational day (GD) 15 reduced the fetal 
      expression of GH from the onset at GD18. In accordance with this, TCDD attenuated 
      the pup weight during the perinatal period. We then examined the effect of TCDD 
      on the serum concentration of corticosterone, which plays a key role in the 
      proliferation of GH-producing cells, and found that TCDD reduces the circulating 
      level of corticosterone in the mothers at GD18 and the male fetuses at GD19. The 
      reduction in fetuses seems to be due to increased inactivation rather than 
      reduced synthesis, because TCDD induces the fetal expression of hepatic enzymes 
      participating in the metabolism of glucocorticoids without changing the 
      expression of steroidogenic proteins in the pituitary-adrenal axis. Supplying 
      corticosterone to TCDD-exposed mothers restored or tended to restore a 
      TCDD-induced reduction in pup weight as well as the levels of pituitary GH mRNA 
      and serum GH. These results suggest that TCDD lowers GH expression and growth 
      retardation owing, at least partially, to a reduction in the circulating level of 
      glucocorticoid in pregnant mothers and their fetuses.
FAU - Hattori, Yukiko
AU  - Hattori Y
AD  - Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, 
      Higashi-ku, Fukuoka, 812-8582, Japan.
FAU - Takeda, Tomoki
AU  - Takeda T
FAU - Fujii, Misaki
AU  - Fujii M
FAU - Taura, Junki
AU  - Taura J
FAU - Ishii, Yuji
AU  - Ishii Y
FAU - Yamada, Hideyuki
AU  - Yamada H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140411
PL  - United States
TA  - Endocrine
JT  - Endocrine
JID - 9434444
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - 9002-72-6 (Growth Hormone)
RN  - W980KJ009P (Corticosterone)
SB  - IM
CIN - Endocrine. 2014 Nov;47(2):354-6. PMID: 24798449
MH  - Adrenocorticotropic Hormone/*blood
MH  - Animals
MH  - Animals, Newborn
MH  - Corticosterone/*blood
MH  - Female
MH  - Fetal Growth Retardation/*chemically induced/metabolism
MH  - Fetus/*drug effects
MH  - Growth Hormone/blood/metabolism
MH  - Male
MH  - *Maternal Exposure
MH  - Pituitary Gland/metabolism
MH  - *Polychlorinated Dibenzodioxins
MH  - Pregnancy
MH  - Rats
MH  - Rats, Wistar
EDAT- 2014/04/12 06:00
MHDA- 2015/06/25 06:00
CRDT- 2014/04/12 06:00
PHST- 2014/01/12 00:00 [received]
PHST- 2014/03/25 00:00 [accepted]
PHST- 2014/04/12 06:00 [entrez]
PHST- 2014/04/12 06:00 [pubmed]
PHST- 2015/06/25 06:00 [medline]
AID - 10.1007/s12020-014-0257-3 [doi]
PST - ppublish
SO  - Endocrine. 2014 Nov;47(2):572-80. doi: 10.1007/s12020-014-0257-3. Epub 2014 Apr 
      11.