ESPE Abstracts

Background: Muscle is key to glucose metabolism. Myogenesis is completed in early infancy, partly under the inhibitory control of myostatin, a myokine whose actions can be influenced by follistatin. Early lowering of myostatin actions is thus a potential strategy to reduce the risk for later diabetes.

Objective and hypotheses: We performed a first screening of whether such lowering is among the natural mechanisms whereby some human infants augment their lean mass.

Method: Body composition (by DXA) and pre-feeding concentrations of circulating glucose, insulin, IGF-I, high-molecular-weight adiponectin (HMW-adip), myostatin and follistatin were assessed longitudinally (at 0 and 4 months) in large-for-gestational-age (LGA, n=30) newborns born from non-diabetic mothers; results were compared to those of infants born appropriate for gestational age (AGA, n=95); all infants were breastfed for >4 mo. In addition, circulating myostatin and follistatin were measured cross-sectionally in ten AGA newborns (mean postnatal age, 35 h) and in 14 pregnant women (mean gestational age, 35 wk) who delivered healthy AGA infants.

Results: LGA, breast-fed infants from non-diabetic mothers were found to switch from an adipose to a lean body composition (with a surplus of lean mass and a normal fat mass) and to an insulin-sensitive state, while having the lowest myostatinemia and follistatinemia so far reported in the human. In the cross-sectional study, myostatinemia and follistatinemia in late-gestational women were the highest so far reported, perhaps contributing to late-gestational adipogenesis. Myostatinemia and follistatinemia in first-week newborns were higher than at birth, suggesting that myostatin and follistatin in the fetal circulation are not of (trans-) placental origin.

Conclusions: Myostatinemia and follistatinemia are extreme in early life and late gestation, and their fetal-neonatal lowering may be among the natural mechanisms whereby some infants augment their myogenesis, potentially for life.