{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:51:37Z","timestamp":1791406297108,"version":"4.3.3"},"reference-count":45,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2016,5,3]],"date-time":"2016-05-03T00:00:00Z","timestamp":1462233600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Metabolism Res"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Animal studies report a nephron deficit in offspring exposed to maternal diabetes, yet are limited to models of severe hyperglycaemia which do not reflect the typical clinical condition and which are associated with foetal growth restriction that may confound nephron endowment. We aimed to assess renal morphology and function in offspring of leptin receptor deficient mice (<jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+) and hypothesized that exposure to impaired maternal glucose tolerance (IGT) would be detrimental to the developing kidney.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Nephron endowment was assessed in offspring of C57BKS\/J <jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+ and +\/+ mice at embryonic day (E)18 and postnatal day (PN)21 using design\u2010based stereology. Transcutaneous measurement of renal function and total glomerular volume were assessed in 6\u2010month\u2010old offspring. Only +\/+ offspring of <jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+ dams were analysed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Compared with +\/+ dams, <jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+ dams had a 20% and 35% decrease in glucose tolerance prior to pregnancy and at E17.5 respectively. Offspring of IGT <jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+ dams had approximately 15% fewer nephrons at E18.5 and PN21 than offspring of +\/+ dams. There was no difference in offspring bodyweight. Despite normal renal function, total glomerular volume was 13% greater in 6\u2010month\u2010old offspring of IGT <jats:italic>Lepr<jats:sup>db<\/jats:sup><\/jats:italic>\/+ dams than in +\/+ offspring.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>IGT throughout gestation resulted in a nephron deficit that was established early in renal development. Maternal IGT was associated with glomerular hypertrophy in adult offspring, likely a compensatory response to maintain normal renal function. Given the increasing prevalence of IGT, monitoring glucose from early in gestation may be important to prevent altered kidney morphology. 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