Volume 90, Issue 6, December (2003), pp. 1023-1029 © The Author 2003
doi:10.1079/BJN2003992

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Early post-hatching starvation delays p70 S6 kinase activation in the muscle of neonatal chicks

Karine Bigot¹, Mohammed Taouis^1,2, Michel Picard¹, Sophie Tesseraud^1
1Régulation du Métabolisme des Oiseaux, Station de Recherches Avicoles, Institut National de la Recherche Agronomique, Centre de Tours-Nouzilly, 37380 Nouzilly, France
²Laboratoire de Biologie Cellulaire et Moléculaire, Biotechnologies, Institut National de la Recherche Agronomique, Domaine de Vilvert, 78352 Jouy-en-Josas, France

 (Received 17 February 2003–Revised 23 June 2003–Accepted 30 July 2003)

Chicken muscle ribosomal protein S6 kinase (S6K1) has been recently characterised and its enzymic activity is regulated by the nutritional and hormonal (insulin) status in vivo. The regulation of S6K1 is still unknown in neonatal chicks. The present study aimed to compare the activation of S6K1 in early-feeding (EF) and 48 h-delayed-feeding (DF) chicks from hatching to 4 d of age. During post-hatching starvation, S6K1 activity remained at the basal level measured in the control-hatched chicks. The maximum S6K1 activity was recorded on the first day of feeding with an increase of about 2·5-fold in the EF and DF chicks (P<0·01). S6K1 activity was correlated with plasma insulin level, suggesting a probable insulin-dependent S6K1 activation. The feeding-induced increase in S6K1 activity was related to its Thr389 residue phosphorylation. A similar pattern for protein kinase B phosphorylation was observed, upstream from S6K1. The S6K1 pathway was stimulated to the same extent in the EF and DF chicks, which indicates that post-hatching starvation did not increase S6K1 activation. It is concluded that muscle S6K1 is activated as soon as food is available without improvement in the response of the S6K1 pathway after post-hatching starvation.

Keywords:
Chicks, Neonatal feeding, p70 S6 kinase activation, Skeletal muscle

Abbreviations:
DF, delayed-feeding, EF, early-feeding, IRS, insulin-receptor substrate, PKB, protein kinase B (also termed Akt), S6K1, p70 S6 kinase, Tris, tri(hydroxymethyl)-aminomethane