Placental expression of myostatin and follistatin like-3 protein in a model of developmental programming

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dc.contributor.author Peiris, Hassendrini en
dc.contributor.author Ponnampalam, Anna en
dc.contributor.author Osepchook, Claire en
dc.contributor.author Mitchell, Murray en
dc.contributor.author Green, Mark en
dc.date.accessioned 2012-03-13T00:20:20Z en
dc.date.issued 2009 en
dc.identifier.citation American journal of physiology. Endocrinology and metabolism 298(4):E854-E861 Apr 2010 en
dc.identifier.issn 0193-1849 en
dc.identifier.uri http://hdl.handle.net/2292/14104 en
dc.description.abstract Placental expression of myostatin and follistatin-like-3 protein in a model of developmental programming. Am J Physiol Endocrinol Metab 298: E854–E861, 2010. First published January 26, 2010; doi:10.1152/ajpendo.00673.2009.—Maternal undernutrition during gestation is known to be detrimental to fetal development, leading to a propensity for metabolic disorders later in the adult lives of the offspring. Identifying possible mediators and physiological processes involved in modulating nutrient transport within the placenta is essential to prevent and/or develop treatments for the effects of aberrant nutrition, nutrient transfer, and detrimental changes to fetal development. A potential role for myostatin as a mediator of nutrient uptake and transport from the mother to the fetus was shown through the recent finding that myostatin acts within the human placenta to modulate glucose uptake and therefore homeostasis. The mRNA and protein expression of myostatin and its inhibitor, follistatin-like-3 (FSTL3), was studied in the placenta and skeletal muscle of a transgenerational Wistar rat model of gestational maternal undernutrition in which the F2 offspring postweaning consumed a high-fat (HF) diet. Alterations in placental characteristics and offspring phenotype, specifically glucose homeostasis, were evident in the transgenerationally undernourished (UNAD) group. Myostatin and FSTL3 protein expression were also higher (P 0.05) in the placentae of the UNAD compared with the control group. At maturity, UNAD HF-fed animals had higher (P 0.05) skeletal muscle expression of FSTL3 than control animals. In summary, maternal undernutrition during gestation results in the aberrant regulation of myostatin and FSTL3 in the placenta and skeletal muscle of subsequent generations. Myostatin, through the disruption of maternal nutrient supply to the fetus, may thus be a potential mediator of offspring phenotype. en
dc.publisher American Physiological Society en
dc.relation.ispartofseries American Journal of Physiology - Endocrinology and Metabolism en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.title Placental expression of myostatin and follistatin like-3 protein in a model of developmental programming en
dc.type Journal Article en
dc.identifier.doi 10.1152/ajpendo.00673.2009 en
pubs.begin-page E854 en
pubs.volume 298 en
dc.rights.holder Copyright: American Physiological Society en
dc.identifier.pmid 20103742 en
pubs.end-page E861 en
dc.rights.accessrights http://purl.org/eprint/accessRights/RestrictedAccess en
pubs.subtype Article en
pubs.elements-id 98970 en
pubs.org-id Medical and Health Sciences en
pubs.org-id Medical Sciences en
pubs.org-id Physiology Division en
pubs.record-created-at-source-date 2010-09-01 en
pubs.dimensions-id 20103742 en


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