POSTER PRESENTATION Open Access Uteroplacental insufficiency decreases forkhead box protein O1A (foxO1a) hepatic levels in perinatal and postnatal IUGR rats Z Shen 1,2,3* , CC Zou 1,2,3 , SQ Shang 1,2,3 , LZ Du 1,2,3 From 7th APPES Biennial Scientific Meeting Nusa Dua, Bali. 14-17 November 2012 Objective IUGR re-programs hepatic gene expression, leading to alterations in perinatal mRNA levels that persist postna- tally. Forkhead bos protein O1a (FoxO1a) is a nclear transcription factor, which is an important regulator of the in vivo metabolism of energetic substance, and play an important role in stabilizing the hepatocyte glucose metabolism and maintaining blood glucose levels in the body. Recent study investigated FoxO1a expression can stimulate key enzymes of gluconeogenesis pathway phos- phoenolpyruvate carboxylase kinases (PEPCK), peroxisome proliferator-activated receptor g auxiliary activating factor- 1a (PGC-1a) and glucose - 6 - phosphatase (G-6-Pase) gene expression. The effect of IUGR upon hepatic FoxO1a expression is unknown. So in this study we investigate the persistent changes in hepatic FoxO1a expression caused by IUGR, which could initiate and maintain the obesity, insulin resistance and type 2 diabetes, and explore whether the changes in FoxO1a expression are gender specific. Methods Dietary restriction was used to induce uteroplacental insufficiency and subsequent IUGR. Control(CON) animals came from dams who received anesthesia. Pups were harvested at d0, d21 and d56 of postnatal life, and liver were harvested. Real-time RT-PCR and Western blotting were used to measure hepatic FoxO1a expression. Results For female and male pups, IUGR significantly decreased FoxO1a hepatic mRNA and protein levels of CON values(P<0.01) at day 0, day21 and at day 56. Conclusions We conclude that IUGR decreases hepatic perinatal and postnatal FoxO1a expression in female and male rats. FoxO1a functions as a nclear transcription factor. Important future studies involve determining which genes are affected by this alteration response to IUGR. Authors’ details 1 Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. 2 Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, Zhejiang, China. 3 Key Laboratory of Reproductive Genetics(Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China. Published: 3 October 2013 doi:10.1186/1687-9856-2013-S1-P208 Cite this article as: Shen et al.: Uteroplacental insufficiency decreases forkhead box protein O1A (foxO1a) hepatic levels in perinatal and postnatal IUGR rats. International Journal of Pediatric Endocrinology 2013 2013(Suppl 1):P208. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space constraints or color ﬁgure charges • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit 1 Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China Full list of author information is available at the end of the article Shen et al. International Journal of Pediatric Endocrinology 2013, 2013(Suppl 1):P208 http://www.ijpeonline.com/content/2013/S1/P208 © 2013 Shen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Uteroplacental insufficiency decreases forkhead box protein O1A (foxO1a) hepatic levels in perinatal and postnatal IUGR rats

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Page 1: Uteroplacental insufficiency decreases forkhead box protein O1A (foxO1a) hepatic levels in perinatal and postnatal IUGR rats

POSTER PRESENTATION Open Access

Uteroplacental insufficiency decreases forkheadbox protein O1A (foxO1a) hepatic levels inperinatal and postnatal IUGR ratsZ Shen1,2,3*, CC Zou1,2,3, SQ Shang1,2,3, LZ Du1,2,3

From 7th APPES Biennial Scientific MeetingNusa Dua, Bali. 14-17 November 2012

ObjectiveIUGR re-programs hepatic gene expression, leading toalterations in perinatal mRNA levels that persist postna-tally. Forkhead bos protein O1a (FoxO1a) is a ncleartranscription factor, which is an important regulator of thein vivo metabolism of energetic substance, and play animportant role in stabilizing the hepatocyte glucosemetabolism and maintaining blood glucose levels in thebody. Recent study investigated FoxO1a expression canstimulate key enzymes of gluconeogenesis pathway phos-phoenolpyruvate carboxylase kinases (PEPCK), peroxisomeproliferator-activated receptor g auxiliary activating factor-1a (PGC-1a) and glucose - 6 - phosphatase (G-6-Pase)gene expression. The effect of IUGR upon hepatic FoxO1aexpression is unknown. So in this study we investigate thepersistent changes in hepatic FoxO1a expression causedby IUGR, which could initiate and maintain the obesity,insulin resistance and type 2 diabetes, and explore whetherthe changes in FoxO1a expression are gender specific.

MethodsDietary restriction was used to induce uteroplacentalinsufficiency and subsequent IUGR. Control(CON)animals came from dams who received anesthesia. Pupswere harvested at d0, d21 and d56 of postnatal life, andliver were harvested. Real-time RT-PCR and Westernblotting were used to measure hepatic FoxO1a expression.

ResultsFor female and male pups, IUGR significantly decreasedFoxO1a hepatic mRNA and protein levels of CONvalues(P<0.01) at day 0, day21 and at day 56.

ConclusionsWe conclude that IUGR decreases hepatic perinatal andpostnatal FoxO1a expression in female and male rats.FoxO1a functions as a nclear transcription factor.Important future studies involve determining whichgenes are affected by this alteration response to IUGR.

Authors’ details1Children’s Hospital, Zhejiang University School of Medicine, Hangzhou,Zhejiang, China. 2Zhejiang Key Laboratory for Diagnosis and Therapy ofNeonatal Diseases, Hangzhou, Zhejiang, China. 3Key Laboratory ofReproductive Genetics(Zhejiang University), Ministry of Education, Hangzhou,Zhejiang, China.

Published: 3 October 2013

doi:10.1186/1687-9856-2013-S1-P208Cite this article as: Shen et al.: Uteroplacental insufficiency decreasesforkhead box protein O1A (foxO1a) hepatic levels in perinatal andpostnatal IUGR rats. International Journal of Pediatric Endocrinology 20132013(Suppl 1):P208.

Submit your next manuscript to BioMed Centraland take full advantage of:

• Convenient online submission

• Thorough peer review

• No space constraints or color figure charges

• Immediate publication on acceptance

• Inclusion in PubMed, CAS, Scopus and Google Scholar

• Research which is freely available for redistribution

Submit your manuscript at www.biomedcentral.com/submit

1Children’s Hospital, Zhejiang University School of Medicine, Hangzhou,Zhejiang, ChinaFull list of author information is available at the end of the article

Shen et al. International Journal of Pediatric Endocrinology 2013, 2013(Suppl 1):P208http://www.ijpeonline.com/content/2013/S1/P208

© 2013 Shen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction inany medium, provided the original work is properly cited.

http://creativecommons.org/licenses/by/2.0