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Myostatin Is a Human Placental Product That Regulates Glucose Uptake

Liggins Institute, University of Auckland (M.D.M., C.C.O., K.-C.L., J.J.B.), and National Research Center for Growth and Development (M.D.M.), Auckland 1003, New Zealand; and Functional Muscle Genomics, AgResearch Ltd., Ruakura Agricultural Center (C.D.M.), Hamilton 2001, New Zealand

Address all correspondence and requests for reprints to: Dr. Murray D. Mitchell, Liggins Institute, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail: m.mitchell{at}auckland.ac.nz.

Abstract

Context: Myostatin is a member of the TGF-ß 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: The objective of this study was to determine whether myostatin is present in and formed by the human placenta and to evaluate its 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 wk), and early in pregnancy (n = 6; 9–13 wk).

Results: Human placentas were shown to express myostatin protein, with a significantly lower expression in term samples compared with samples collected in preterm samples. Human placentas 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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