Please use this identifier to cite or link to this item:
Title: The Placental Variant of Human Growth Hormone Reduces Maternal Insulin Sensitivity in a Dose-Dependent Manner in C57BL/6J Mice.
Authors: Liao, S.
Vickers, M. H.
Stanley, J. L.
Ponnampalam, A. P.
Baker, Philip Newton
Perry, J. K.
First Published: 15-Dec-2015
Publisher: Endocrine Society
Citation: Endocrinology, 2016, 157 (3), pp. 1175-1186
Abstract: The human placental GH variant (GH-V) is secreted continuously from the syncytiotrophoblast layer of the placenta during pregnancy and is thought to play a key role in the maternal adaptation to pregnancy. Maternal GH-V concentrations are closely related to fetal growth in humans. GH-V has also been proposed as a potential candidate to mediate insulin resistance observed later in pregnancy. To determine the effect of maternal GH-V administration on maternal and fetal growth and metabolic outcomes during pregnancy, we examined the dose-response relationship for GH-V administration in a mouse model of normal pregnancy. Pregnant C57BL/6J mice were randomized to receive vehicle or GH-V (0.25, 1, 2, or 5 mg/kg · d) by osmotic pump from gestational days 12.5 to 18.5. Fetal linear growth was slightly reduced in the 5 mg/kg dose compared with vehicle and the 0.25 mg/kg groups, respectively, whereas placental weight was not affected. GH-V treatment did not affect maternal body weights or food intake. However, treatment with 5 mg/kg · d significantly increased maternal fasting plasma insulin concentrations with impaired insulin sensitivity observed at day 18.5 as assessed by homeostasis model assessment. At 5 mg/kg · d, there was also an increase in maternal hepatic GH receptor/binding protein (Ghr/Ghbp) and IGF binding protein 3 (Igfbp3) mRNA levels, but GH-V did not alter maternal plasma IGF-1 concentrations or hepatic Igf-1 mRNA expression. Our findings suggest that at higher doses, GH-V treatment can cause hyperinsulinemia and is a likely mediator of the insulin resistance associated with late pregnancy.
DOI Link: 10.1210/en.2015-1718
ISSN: 0013-7227
eISSN: 1945-7170
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2016 by the Endocrine Society. Deposited with reference to the publisher’s archiving policy available on the SHERPA/RoMEO website.
Appears in Collections:Published Articles, College of Medicine, Biological Sciences and Psychology

Files in This Item:
File Description SizeFormat 
Manusript 13-7-15 st..docPost-review (final submitted)258 kBMicrosoft WordView/Open
Supplementary Figure 1.pptxPost-review (final submitted)800.72 kBUnknownView/Open
Table 13-7-15 st.docxPost-review (final submitted)22.65 kBUnknownView/Open
Manusript 13-7-15 st..pdfPost-review (final submitted)403.02 kBAdobe PDFView/Open
Supplementary Figure 1.pdfPost-review (final submitted)230.19 kBAdobe PDFView/Open
Table 13-7-15 st.pdfPost-review (final submitted)107.47 kBAdobe PDFView/Open

Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.