ESPE Abstracts (2014) 82 P-D-2-2-378

Circulating Concentrations of Fibroblast Growth Factor 21 are Undetectable in Human Infants at Term Birth and Surge within Hours After Birth

David Sánchez-Infantesa,c, José Miguel Gallego-Escuderob, Rubén Cereijob, Marta Díaza,c, Gemma Aragonésa, Abel López-Bermejod, Francis de Zeghere, Francesc Villarroyab & Lourdes Ibáñeza,c


aSant Joan de Deu Hospital, Barcelona, Spain; bUniversity of Barcelona, Barcelona, Spain; cCIBERDEM–ISCIII, Madrid, Spain; dDr Josep Trueta Hospital, Girona, Spain; eUniversity of Leuven, Leuven, Belgium


Background: In rodents, fibroblast growth factor 21 (FGF21), an endocrine member of the FGF family, is mainly produced in the liver and promotes glucose oxidation in several tissues; the circulating concentrations of FGF21 rise shortly after birth. In the human, the ontogeny of circulating FGF21 is essentially unknown.

Objective and hypotheses: To assess whether there is also a neonatal surge of circulating FGF21 concentrations in human infants and, if any, whether FGF21 concentrations in human infants relate to their prenatal growth (as judged by birthweight for gestational age), to body composition (as judged by neonatal absorptiometry) and to insulin resistance (as judged by HOMA-IR calculated from prefeeding glycaemia and insulinaemia).

Method: Concentrations of circulating FGF21 were measured longitudinally (birth, 4 and 12 months) in 66 term infants (22 born small-, 22 appropriate-, and 22 large-for-gestational-age; SGA, AGA, and LGA) and cross-sectionally in first-week newborns (n=10; 1–4 days).

Results: Circulating FGF21 was not detectable in human infants at term birth but was readily detectable in first-week newborns. FGF21 concentrations in infants aged 4 or 12 months compared to those in first-week newborns, were similar in girls and boys, similar in SGA, AGA, and LGA infants, and were ~1.4-fold higher than those previously described in adults (P<0.0001). In SGA infants aged 4 months, circulating FGF21 associated negatively to HOMA-IR (P=0.001), but not to birthweight or body composition variables.

Conclusion: Pilot evidence suggests that there is a neonatal surge of circulating FGF21 in human infants. The mechanisms underpinning this neonatal surge remain to be disclosed but may involve the neonatal initiation of enteral nutrition as well as neonatal changes in hepatic perfusion and/or metabolism.