{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T04:35:40Z","timestamp":1790742940378,"version":"4.1.0"},"reference-count":51,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p>\n                    Epidemiological studies demonstrate that the link between impaired fetal development and glucose intolerance in later life is exacerbated by postnatal catch-up growth. Maternal protein restriction (MPR) during pregnancy and lactation in the rat has been previously demonstrated to lead to impaired glucose tolerance in adulthood, however the effects of protein restoration during weaning on glucose homeostasis are largely unknown. Recent\n                    <jats:italic>in vitro<\/jats:italic>\n                    studies have identified that the liver X receptor \u03b1 (LXR\u03b1) maintains glucose homeostasis by inhibiting critical genes involved in gluconeogenesis including\n                    <jats:italic>G6pase<\/jats:italic>\n                    (\n                    <jats:italic>G6pc<\/jats:italic>\n                    ),\n                    <jats:italic>11<\/jats:italic>\n                    <jats:italic>\u03b2<\/jats:italic>\n                    <jats:italic>-Hsd1<\/jats:italic>\n                    (\n                    <jats:italic>Hsd11b1<\/jats:italic>\n                    ) and\n                    <jats:italic>Pepck<\/jats:italic>\n                    (\n                    <jats:italic>Pck1<\/jats:italic>\n                    ). Therefore, we hypothesized that MPR with postnatal catch-up growth would impair LXR\u03b1\n                    <jats:italic>in vivo<\/jats:italic>\n                    , which in turn would lead to augmented gluconeogenic LXR\u03b1-target gene expression and glucose intolerance. To examine this hypothesis, pregnant Wistar rats were fed a control (20%) protein diet (C) or a low (8%) protein diet during pregnancy and switched to a control diet at birth (LP). At 4 months, the LP offspring had impaired glucose tolerance. In addition, LP offspring had decreased LXR\u03b1 expression, while hepatic expression of 11\u03b2-HSD1 and G6Pase was significantly higher. This was concomitant with decreased binding of LXR\u03b1 to the putative LXRE on\n                    <jats:italic>11<\/jats:italic>\n                    <jats:italic>\u03b2<\/jats:italic>\n                    <jats:italic>-Hsd1<\/jats:italic>\n                    and\n                    <jats:italic>G6pase<\/jats:italic>\n                    . Finally, we demonstrated that the acetylation of histone H3 (K9,14) surrounding the transcriptional start site of hepatic\n                    <jats:italic>Lxr<\/jats:italic>\n                    <jats:italic>\u03b1<\/jats:italic>\n                    (\n                    <jats:italic>Nr1h3<\/jats:italic>\n                    ) was decreased in LP offspring, suggesting MPR-induced epigenetic silencing of the\n                    <jats:italic>Lxr<\/jats:italic>\n                    <jats:italic>\u03b1<\/jats:italic>\n                    promoter. In summary, our study demonstrates for the first time the important role of LXR\u03b1 in mediating enhanced hepatic gluconeogenic gene expression and consequent glucose intolerance in adult MPR offspring.\n                  <\/jats:p>","DOI":"10.1530\/joe-13-0055","type":"journal-article","created":{"date-parts":[[2013,5,1]],"date-time":"2013-05-01T08:21:59Z","timestamp":1367396519000},"page":"85-97","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":54,"title":["Maternal protein restriction leads to enhanced hepatic gluconeogenic gene expression in adult male rat offspring due to impaired expression of the liver X receptor"],"prefix":"10.1530","volume":"218","author":[{"given":"Thin Xuan","family":"Vo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Revesz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gurjeev","family":"Sohi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noelle","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel B","family":"Hardy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"issue":"10","key":"1_15633834","doi-asserted-by":"crossref","first-page":"7025","DOI":"10.1128\/MCB.14.10.7025","volume":"14","author":"Apfel","year":"1994","journal-title":"Molecular and Cellular Biology","ISSN":"https:\/\/id.crossref.org\/issn\/0270-7306","issn-type":"print"},{"issue":"1","key":"2_10144214","doi-asserted-by":"publisher","first-page":"62","DOI":"10.1007\/BF00399095","volume":"36","author":"Barker","year":"1993","journal-title":"Diabetologia","ISSN":"https:\/\/id.crossref.org\/issn\/0012-186X","issn-type":"print"},{"issue":"3","key":"3_23685640","doi-asserted-by":"publisher","first-page":"435","DOI":"10.1017\/S0007114507352392","volume":"97","author":"Burdge","year":"2007","journal-title":"The British journal of nutrition","ISSN":"https:\/\/id.crossref.org\/issn\/0007-1145","issn-type":"print"},{"issue":"7","key":"4_5751037","doi-asserted-by":"crossref","first-page":"1768","DOI":"10.1172\/JCI119703","volume":"100","author":"Burns","year":"1997","journal-title":"Journal of Clinical Investigation","ISSN":"https:\/\/id.crossref.org\/issn\/0021-9738","issn-type":"print"},{"issue":"2","key":"5_19560980","doi-asserted-by":"publisher","first-page":"1131","DOI":"10.1074\/jbc.M210208200","volume":"278","year":"2003","journal-title":"Journal of Biological Chemistry","ISSN":"https:\/\/id.crossref.org\/issn\/0021-9258","issn-type":"print"},{"issue":"13","key":"6_18924036","doi-asserted-by":"publisher","first-page":"2933","DOI":"10.1093\/bioinformatics\/bti473","volume":"21","year":"2005","journal-title":"Bioinformatics","ISSN":"https:\/\/id.crossref.org\/issn\/1367-4803","issn-type":"print"},{"issue":"1","key":"7_9687682","doi-asserted-by":"crossref","first-page":"217","DOI":"10.1242\/dev.113.1.217","volume":"113","author":"Cascio","year":"1991","journal-title":"Development","ISSN":"https:\/\/id.crossref.org\/issn\/0950-1991","issn-type":"print"},{"issue":"12","key":"8_45847525","doi-asserted-by":"publisher","first-page":"1425","DOI":"10.3181\/0902-RM-69","volume":"234","author":"Chamson-Reig","year":"2009","journal-title":"Experimental Biology and Medicine","ISSN":"https:\/\/id.crossref.org\/issn\/1535-3702","issn-type":"print"},{"issue":"3","key":"9_34425184","doi-asserted-by":"publisher","first-page":"e4950","DOI":"10.1371\/journal.pone.0004950","volume":"4","author":"Chen","year":"2009","ISSN":"https:\/\/id.crossref.org\/issn\/1932-6203","issn-type":"print"},{"issue":"8","key":"10_20134088","doi-asserted-by":"publisher","first-page":"871","DOI":"10.1001\/archpedi.1991.02160080047019","volume":"145","author":"Crosby","year":"1991","journal-title":"Archives of Pediatrics and Adolescent Medicine","ISSN":"https:\/\/id.crossref.org\/issn\/0096-8994","issn-type":"print"},{"issue":"2","key":"11_16785381","doi-asserted-by":"crossref","first-page":"329","DOI":"10.1017\/S0006323196005026","volume":"72","author":"Desai","year":"1997","journal-title":"Biological Reviews (Cambridge; Print)","ISSN":"https:\/\/id.crossref.org\/issn\/1469-185X","issn-type":"print"},{"issue":"2","key":"12_16006542","doi-asserted-by":"crossref","first-page":"331","DOI":"10.1042\/bst0230331","volume":"23","author":"Desai","year":"1995","journal-title":"Biochemical Society Transactions","ISSN":"https:\/\/id.crossref.org\/issn\/1470-8752","issn-type":"print"},{"issue":"4","key":"13_31297871","doi-asserted-by":"publisher","first-page":"257","DOI":"10.1055\/s-2008-1058064","volume":"40","author":"Dutriez-Casteloot","year":"2008","journal-title":"Hormone and metabolic research. 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