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LIN28A/B are RNA binding proteins implicated by genetic association studies in human growth and glucose metabolism. Mice with ectopic over‐expression of  Lin28a  have shown related phenotypes. Here, we describe the first comprehensive analysis of the physiologic consequences of  Lin28a  and  Lin28b  deficiency in knockout (KO) mice.  Lin28a/b ‐deficiency led to dwarfism starting at different ages, and compound gene deletions showed a cumulative dosage effect on organismal growth. Conditional gene deletion at specific developmental stages revealed that fetal but neither neonatal nor adult deficiency resulted in growth defects and aberrations in glucose metabolism. Tissue‐specific KO mice implicated skeletal muscle‐deficiency in the abnormal programming of adult growth and metabolism. The effects of  Lin28b  KO could be rescued by  Tsc1  haplo‐insufficiency in skeletal muscles. Our data implicate fetal expression of  Lin28a/b  in the regulation of life‐long effects on metabolism and growth, and demonstrate that fetal  Lin28b  acts at least in part via mTORC1 signaling.  S TEM  C ells  2013;31:1563–1573

Fetal Deficiency of Lin28 Programs Life‐Long Aberrations in Growth and Glucose Metabolism