Abstract：
:At birth the trans-placental nutrient supply is suddenly interrupted, and neonates face severe starvation until supply can be restored through milk nutrients. Here, we show that neonates adapt to this adverse circumstance by inducing autophagy. Autophagy is the primary means for the degradation of cytoplasmic constituents within lysosomes. The level of autophagy in mice remains low during embryogenesis; however, autophagy is immediately upregulated in various tissues after birth and is maintained at high levels for 3-12 h before returning to basal levels within 1-2 days. Mice deficient for Atg5, which is essential for autophagosome formation, appear almost normal at birth but die within 1 day of delivery. The survival time of starved Atg5-deficient neonates (approximately 12 h) is much shorter than that of wild-type mice (approximately 21 h) but can be prolonged by forced milk feeding. Atg5-deficient neonates exhibit reduced amino acid concentrations in plasma and tissues, and display signs of energy depletion. These results suggest that the production of amino acids by autophagic degradation of 'self' proteins, which allows for the maintenance of energy homeostasis, is important for survival during neonatal starvation.
journal_name
Naturejournal_title
Natureauthors
Kuma A,Hatano M,Matsui M,Yamamoto A,Nakaya H,Yoshimori T,Ohsumi Y,Tokuhisa T,Mizushima Ndoi
10.1038/nature03029keywords:
subject
Has Abstractpub_date
2004-12-23 00:00:00pages
1032-6issue
7020eissn
0028-0836issn
1476-4687pii
nature03029journal_volume
432pub_type
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