Secular trend for increasing birthweight in offspring of pregnant women with type 1 diabetes: is improved placentation the reason?

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Despite enormous progress in managing blood glucose levels, pregnancy in women with type 1 diabetes still carries risks for the growing fetus. While, previously, fetal undergrowth was not uncommon in these women, with improved maternal glycaemic control we now see an increased prevalence of fetal overgrowth. Besides short-term implications, offspring of women with type 1 diabetes are more likely to become obese and to develop diabetes and features of the metabolic syndrome. Here, we argue that the increase in birthweight is paradoxically related to improved glycaemic control in the pre- and periconceptional periods. Good glycaemic control reduces the prevalence of microangiopathy and improves placentation in early pregnancy, which may lead to unimpeded fetal nutrition. Even mild maternal hyperglycaemia may then later result in fetal overnutrition. This notion is supported by circumstantial evidence that lower HbA1c levels as well as increases in markers of placental size and function in early pregnancy are associated with large-for-gestational age neonates. We also emphasise that neonates with normal birthweight can have excessive fat deposition. This may occur when poor placentation leads to initial fetal undergrowth, followed by fetal overnutrition due to maternal hyperglycaemia. Thus, the complex interaction of glucose levels during different periods of pregnancy ultimately determines the risk of adiposity, which can occur in fetuses with both normal and elevated birthweight. Prevention of fetal adiposity calls for revised goal setting to enable pregnant women to maintain blood glucose levels that are closer to normal. This could be supported by continuous glucose monitoring throughout pregnancy and appropriate maternal gestational weight gain. Future research should consider the measurement of adiposity in neonates. Graphical abstract: [Figure not available: see fulltext.].

OriginalsprogEngelsk
TidsskriftDiabetologia
Vol/bind66
Sider (fra-til)33–43
Antal sider11
ISSN0012-186X
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
Open access funding provided by Medical University of Graz. GD was supported by a visiting professorship grant from the Danish Diabetes Academy, which is funded by the Novo Nordisk Foundation (grant number NNF17SA0031406). Work in GD’s laboratory is supported by the Oesterreichische Nationalbank (Anniversary Fund, project number 17950). The funders were not involved in the writing of the manuscript and did not impose any restrictions regarding its publication.

Publisher Copyright:
© 2022, The Author(s).

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