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In addition, low birthweight associates with adult diseases including hypertension, metabolic dysfunction and behavioural disorders. A key mechanism underlying <jats:styled-content style=\"fixed-case\">FGR<\/jats:styled-content> is exposure of the foetus to glucocorticoids which, while critical for foetal development, in excess can reduce foetal growth and permanently alter organ structure and function, predisposing to disease in later life. Foetal glucocorticoid exposure is regulated, at least in part, by the enzyme 11<jats:italic>\u03b2<\/jats:italic>\u2010hydroxysteroid dehydrogenase type 2 (11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2), which catalyses the intracellular inactivation of glucocorticoids. This enzyme is highly expressed within the placenta at the maternal\u2013foetal interface, limiting the passage of glucocorticoids to the foetus. Expression of 11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2 is also high in foetal tissues, particularly within the developing central nervous system. Down\u2010regulation or genetic deficiency of placental 11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2 is associated with significant reductions in foetal growth and birth weight, and programmed outcomes in adulthood. To unravel the direct significance of 11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2 for developmental programming, placental function, neurodevelopment and adult behaviour have been extensively investigated in a mouse knockout of 11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2. This review highlights the evidence obtained from this mouse model for a critical role of feto\u2010placental 11<jats:italic>\u03b2<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">HSD<\/jats:styled-content>2 in determining the adverse programming outcomes.<\/jats:p>","DOI":"10.1111\/apha.12187","type":"journal-article","created":{"date-parts":[[2013,10,28]],"date-time":"2013-10-28T09:34:58Z","timestamp":1382952898000},"page":"288-295","source":"Crossref","is-referenced-by-count":109,"title":["Foetal and placental 11<i>\u03b2<\/i>\u2010<scp>HSD<\/scp>2: a hub for developmental programming"],"prefix":"10.1111","volume":"210","author":[{"given":"E. C.","family":"Cottrell","sequence":"first","affiliation":[{"name":"Maternal and Fetal Health Research Centre Institute of Human Development University of Manchester Manchester UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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