PMID- 25625347
OWN - NLM
STAT- MEDLINE
DCOM- 20160304
LR  - 20181113
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Print)
IS  - 0022-3751 (Linking)
VI  - 593
IP  - 5
DP  - 2015 Mar 1
TI  - Corticosterone alters materno-fetal glucose partitioning and insulin signalling 
      in pregnant mice.
PG  - 1307-21
LID - 10.1113/jphysiol.2014.287177 [doi]
AB  - Glucocorticoids affect glucose metabolism in adults and fetuses, although their 
      effects on materno-fetal glucose partitioning remain unknown. The present study 
      measured maternal hepatic glucose handling and placental glucose transport 
      together with insulin signalling in these tissues in mice drinking corticosterone 
      either from day (D) 11 to D16 or D14 to D19 of pregnancy (term = D21). On the 
      final day of administration, corticosterone-treated mice were hyperinsulinaemic 
      (P < 0.05) but normoglycaemic compared to untreated controls. In maternal liver, 
      there was no change in glycogen content or glucose 6-phosphatase activity but 
      increased Slc2a2 glucose transporter expression in corticosterone-treated mice, 
      on D16 only (P < 0.05). On D19, but not D16, transplacental (3) 
      H-methyl-d-glucose clearance was reduced by 33% in corticosterone-treated dams (P 
      < 0.05). However, when corticosterone-treated animals were pair-fed to control 
      intake, aiming to prevent the corticosterone-induced increase in food 
      consumption, (3) H-methyl-d-glucose clearance was similar to the controls. 
      Depending upon gestational age, corticosterone treatment increased 
      phosphorylation of the insulin-signalling proteins, protein kinase B (Akt) and 
      glycogen synthase-kinase 3beta, in maternal liver (P < 0.05) but not placenta (P > 
      0.05). Insulin receptor and insulin-like growth factor type I receptor abundance 
      did not differ with treatment in either tissue. Corticosterone upregulated the 
      stress-inducible mechanistic target of rapamycin (mTOR) suppressor, Redd1, in 
      liver (D16 and D19) and placenta (D19), in ad libitum fed animals (P < 0.05). 
      Concomitantly, hepatic protein content and placental weight were reduced on D19 
      (P < 0.05), in association with altered abundance and/or phosphorylation of 
      signalling proteins downstream of mTOR. Taken together, the data indicate that 
      maternal glucocorticoid excess reduces fetal growth partially by altering 
      placental glucose transport and mTOR signalling.
CI  - (c) 2015 The Authors. The Journal of Physiology (c) 2015 The Physiological Society.
FAU - Vaughan, O R
AU  - Vaughan OR
AD  - Centre for Trophoblast Research, Department of Physiology, Development and 
      Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK.
FAU - Fisher, H M
AU  - Fisher HM
FAU - Dionelis, K N
AU  - Dionelis KN
FAU - Jeffreys, E C
AU  - Jeffreys EC
FAU - Higgins, J S
AU  - Higgins JS
FAU - Musial, B
AU  - Musial B
FAU - Sferruzzi-Perri, A N
AU  - Sferruzzi-Perri AN
FAU - Fowden, A L
AU  - Fowden AL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150129
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Blood Glucose)
RN  - 0 (Ddit4 protein, mouse)
RN  - 0 (Insulin)
RN  - 0 (Transcription Factors)
RN  - 9005-79-2 (Glycogen)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Gsk3b protein, mouse)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
RN  - W980KJ009P (Corticosterone)
SB  - IM
EIN - J Physiol. 2016 Sep 1;594(17 ):5033. PMID: 27581573
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Blood Glucose/*metabolism
MH  - Corticosterone/*pharmacology
MH  - Eating
MH  - Female
MH  - Fetal Blood/metabolism
MH  - Glycogen/metabolism
MH  - Glycogen Synthase Kinase 3/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Insulin/blood/*metabolism
MH  - Liver/metabolism
MH  - Maternal-Fetal Exchange/*drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Placenta/metabolism
MH  - Pregnancy
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - *Signal Transduction
MH  - Transcription Factors/genetics/metabolism
PMC - PMC4358686
EDAT- 2015/01/28 06:00
MHDA- 2016/03/05 06:00
PMCR- 2016/03/01
CRDT- 2015/01/28 06:00
PHST- 2014/11/11 00:00 [received]
PHST- 2014/12/24 00:00 [accepted]
PHST- 2015/01/28 06:00 [entrez]
PHST- 2015/01/28 06:00 [pubmed]
PHST- 2016/03/05 06:00 [medline]
PHST- 2016/03/01 00:00 [pmc-release]
AID - 10.1113/jphysiol.2014.287177 [doi]
PST - ppublish
SO  - J Physiol. 2015 Mar 1;593(5):1307-21. doi: 10.1113/jphysiol.2014.287177. Epub 
      2015 Jan 29.