{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T10:01:30Z","timestamp":1790416890397,"version":"4.1.0"},"reference-count":55,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,9,18]],"date-time":"2013-09-18T00:00:00Z","timestamp":1379462400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>\n                      Disruption to insulin\u2010like growth factor (\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      ) signalling pathways during early life causes growth retardation and defects of developing metabolic organs that can alter set points of energy homeostasis for a lifetime. Inheritance of two maternal copies of human chromosome 14q32.2 (\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      emple syndrome) causes severe foetal growth retardation and post\u2010natal failure to thrive. Disruption of imprinted gene dosage in the orthologous region on mouse chromosome 12 also affects growth. Here, we investigated whether altering chromosome 12\u2010imprinted gene dosage can affect\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      signalling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We investigated mice with a transgene insertion at the imprinted domain of chromosome 12. This lesion causes misexpression of neighbouring genes such that the expression of non\u2010coding\n                      <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                      s is elevated, and levels of delta\u2010like homologue 1 (\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                        lk1\n                      <\/jats:italic>\n                      ), retrotransposon\u2010like 1 (\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\n                        tl1\n                      <\/jats:italic>\n                      ) and deiodinase 3 (\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                        io3\n                      <\/jats:italic>\n                      ) transcripts are reduced.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We observed three key phenotypes in these mice: (i) embryonic growth retardation associated with altered expression of\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      1 binding proteins, (ii) peri\u2010natal failure to thrive accompanied by hypothyroidism and low serum\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      1. Unexpectedly this phenotype was growth hormone independent. (iii) Adult animals had reduced glucose tolerance as a result of endocrine pancreatic insufficiency.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      We propose that all of these phenotypes are attributable to impaired\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      action and show for the first time that the chromosome 12 cluster in the mouse is an imprinted locus that modulates the\n                      <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                      signalling pathway. We propose that growth retardation observed in human\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      emple syndrome might have a similar cause.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.12160","type":"journal-article","created":{"date-parts":[[2013,8,23]],"date-time":"2013-08-23T02:52:52Z","timestamp":1377226372000},"page":"174-187","source":"Crossref","is-referenced-by-count":15,"title":["Perturbations to the\n                    <scp>IGF<\/scp>\n                    1 growth pathway and adult energy homeostasis following disruption of mouse chromosome 12 imprinting"],"prefix":"10.1111","volume":"210","author":[{"given":"M.","family":"Charalambous","sequence":"first","affiliation":[{"name":"Department of Physiology, Development and Neuroscience University of Cambridge Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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