Abstract
Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.
Highlights
IGDMtr had higher fat mass (FM) and %FM compared to infants exposed to normal glucose tolerance (INGT), but there was no significant difference in subcutaneous adiposity as measured by skinfold thickness (SFT)
One of the studies included in our review [7] reported that treatment with insulin in addition to lifestyle modification significantly increased the FM and %FM in IGDMtr as opposed to lifestyle intervention alone; the authors speculated that there might have been a confounding effect of other maternal factors associated with increased infant adiposity, as the former group of mothers were characterised with higher pre-pregnancy weight and parity than their counterparts
One study reported a significant increase in intrahepatocellular lipid content in IGDMtr compared to INGT, while the other did not detect such a difference
Summary
As well as causing complications during pregnancy and delivery including macrosomia, shoulder dystocia and preterm birth, exposure to GDM in utero places offspring at an increased risk of obesity and type 2 diabetes in later life [2,3]. The mechanisms associated with this increased risk of obesity and type 2 diabetes are not well understood; increased adiposity during foetal growth has been suggested as a potential mediator [4]. The Pedersen hypothesis [5] suggests that, as glucose freely crosses the placenta, maternal hyperglycaemia in diabetic pregnancies leads to foetal hyperinsulinaemia, causing accelerated foetal uptake of glucose (foetal glucose steal phenomenon) and deposition of excess foetal adipose tissue [6]. The impact of GDM on adipose tissue growth in the foetus can be identified with adiposity measures at birth, for example, fat mass (FM), percent fat mass (%FM) and skinfold thickness (SFT) [7]
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