{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T13:36:08Z","timestamp":1788183368358,"version":"build-2803163510"},"reference-count":78,"publisher":"American Diabetes Association","issue":"8","license":[{"start":{"date-parts":[[2018,7,20]],"date-time":"2018-07-20T00:00:00Z","timestamp":1532044800000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/www.diabetesjournals.org\/content\/license"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,8,1]]},"abstract":"<jats:p>Despite significant reductions in serious adverse perinatal outcomes for women with type 1 diabetes in pregnancy, the opposite effect has been observed for fetal overgrowth and associated complications, such as neonatal hypoglycemia, shoulder dystocia, and admission to the neonatal intensive care unit. In addition, infants born large for gestational age (LGA) have an increased lifetime risk of obesity, diabetes, and chronic disease. Although exposure to hyperglycemia plays an important role, women who seemingly achieve adequate glycemic control in pregnancy continue to experience a greater risk of excess fetal growth, leading to LGA neonates and macrosomia. We review potential contributors to excess fetal growth in pregnancies complicated by type 1 diabetes. In addition to hyperglycemia, we explore the role of glycemic variability, prepregnancy overweight and obesity, gestational weight gain, and maternal lipid levels. Greater understanding of the stimuli that drive excess fetal growth could lead to targeted management strategies in pregnant women with type 1 diabetes, potentially reducing the incidence of LGA neonates and the inherent risk of acute and long-term complications.<\/jats:p>","DOI":"10.2337\/dc18-0551","type":"journal-article","created":{"date-parts":[[2018,7,20]],"date-time":"2018-07-20T19:36:41Z","timestamp":1532115401000},"page":"1821-1828","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":63,"title":["Large-for-Gestational-Age Neonates in Type 1 Diabetes and Pregnancy: Contribution of Factors Beyond Hyperglycemia"],"prefix":"10.2337","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3453-058X","authenticated-orcid":false,"given":"Rachel T.","family":"McGrath","sequence":"first","affiliation":[{"name":"Department of Diabetes, Endocrinology & Metabolism and the Northern Clinical School, Faculty of Medicine and Health, The University of Sydney, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia"},{"name":"Kolling Institute, St Leonards, Sydney, New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah J.","family":"Glastras","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Endocrinology & Metabolism and the Northern Clinical School, Faculty of Medicine and Health, The University of Sydney, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia"},{"name":"Kolling Institute, St Leonards, Sydney, New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2514-9392","authenticated-orcid":false,"given":"Samantha L.","family":"Hocking","sequence":"additional","affiliation":[{"name":"Central Clinical School and The Boden Institute of Obesity, Nutrition, Exercise & Eating Disorders, Faculty of Medicine and Health, Charles Perkins 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