{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T07:06:20Z","timestamp":1762067180736},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"3_Suppl","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1986,8]]},"abstract":"<jats:p>Abstract. Female Sprague-Dawley rats from two different substrains (denoted U and H rats) were made manifest diabetic (MD) with a single iv injection of streptozotocin 2\u20134 weeks before mating. In some MD animals insulin treatment was started 1\u20133 weeks before mating (denoted MDI rats) and in a majority of these animals the treatment was interrupted during two days of pregnancy, i.e. gestational days 2 + 3, 4 + 5, 6 + 7, 8 + 9 or 10 + 11. The pregnant rats were killed on gestational day 20. The offspring of MD and MDI rats of the U substrain showed skeletal malformations (micrognathia and sacral dysgenesis) at a rate up to 19%, whereas the MD and MDI fetuses of the H strain did not display any skeletal malformations. Offspring of the U strain with sacral dysgenesis exhibited lack of a tail and no staining of osseous and cartilagenous tissue in the sacral-caudal region, suggesting total absence of vertebrae. The offspring of the dibetic U rats tended to be more readily resorbed, were smaller and tended to have slightly larger placentae than those of the diabetic H rats. The severity of the diabetic state in pregnant and nonpregnant female rats \u2013 as reflected by body and kidney weights, blood levels of HbA<jats:sub>1c<\/jats:sub>, carbohydrate and lipid metabolites \u2013 did not differ significantly between the U and H rats. These results are in concert with the notion that congenital malformations result from a teratogenic insult in a genetically predisposed organism. The described malformation-prone rat strain (U) may be a suitable model for the future elucidation of teratological mechanisms in diabetic pregnancy.<\/jats:p>","DOI":"10.1530\/acta.0.111s0066","type":"journal-article","created":{"date-parts":[[2009,10,21]],"date-time":"2009-10-21T22:39:20Z","timestamp":1256164760000},"page":"S66-S73","update-policy":"http:\/\/dx.doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":19,"title":["Diabetes in pregnancy: influence of genetic background and maternal diabetic state on the incidence of skeletal malformations in the fetal rat"],"prefix":"10.1093","volume":"113","author":[{"given":"Ulf J.","family":"Eriksson","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V. Elisabeth","family":"Dahlstr\u00f6m","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans O.","family":"Lithell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","container-title":["Acta Endocrinologica"],"original-title":[],"link":[{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/113\/3_Suppl\/acta_111_Suppl_277_011.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/113\/3_Suppl\/acta_111_Suppl_277_011.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,14]],"date-time":"2023-02-14T16:24:39Z","timestamp":1676391879000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ejendo\/article\/113\/3_Supplement\/S66\/6768254"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1986,8]]},"references-count":0,"journal-issue":{"issue":"3_Suppl"},"URL":"https:\/\/doi.org\/10.1530\/acta.0.111s0066","relation":{},"ISSN":["0804-4643","1479-683X"],"issn-type":[{"value":"0804-4643","type":"print"},{"value":"1479-683X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1986,8]]}}}