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Submitted on October 27, 2005
Accepted on January 27, 2006
Liggins Institute, University of Auckland, National Research Centre for Growth and Development, Private Bag 92019, Auckland, New Zealand & Functional Muscle Genomics, AgResearch Limited, Ruakura Agricultural Centre, Hamilton, New Zealand
Context: Myostatin is a member of the transforming growth factor-
superfamily and is primarily known for its ability to inhibit muscle growth. It also has actions on glucose metabolism. We hypothesized that it may act as a paracrine regulator of glucose uptake in the placenta potentially contributing to fetal and placental growth. Objectives: To determine if myostatin is present in and formed by human placentae and to evaluate it's effects on glucose uptake. Materials and Methods: Myostatin protein and mRNA were measured using western immunoblotting and real time PCR respectively. Glucose uptake was assessed by uptake of radiolabeled deoxyglucose in vitro. Placental tissues were obtained at term (n = 8), preterm (n = 8, 24-34 weeks) and early in pregnancy (n = 6, 9-13 weeks). Results: Human placentae were shown to express myostatin protein, with a significantly lower expression in term samples compared with samples collected in preterm. Human placentae express myostatin mRNA throughout gestation which does not change. Myostatin treatment of human term placental explants resulted in an increase in deoxyglucose uptake compared with controls. Conclusions: Myostatin is synthesized, released and acts within the human placenta. It contributes to placental glucose homeostasis and may be a therapeutic target in diseases ranging from placental insufficiency to diabetes in pregnancy.
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