Obesity and abnormal glucose tolerance in offspring of diabetic mothers: A systematic review and meta-analysis

Abstract

BackgroundRising prevalence of childhood obesity and type 2 diabetes mellitus (T2DM) is an emerging public health issue.ObjectivesTo investigate the association of maternal hyperglycemia exposure during pregnancy with obesity and abnormal glucose tolerance in offspring, and the age at occurrence.MethodsWe searched MEDLINE and EMBASE for observational studies on obesity and diabetes in offspring of diabetic mothers (gestational diabetes mellitus (GDM), type 1 diabetes mellitus (T1DM) and T2DM), and those on non-diabetic mothers. We performed fixed effect meta-analysis for all studies except when heterogeneity was detected. The quality of studies was evaluated using the Risk of Bias Assessment Tool for Nonrandomized Studies (RoBANS)ResultsTwenty observational studies were included involving a total of 26,509 children. Offspring of GDM mother had higher BMI z-score in childhood (pooled MD: 0.14, 95%CI: 0.04–0.24, seven studies, 21,691children, low quality of evidence). Offspring of T1DM mothers had higher BMI z-score from prepubertal to adolescent (pooled MD: 0.35, 95% CI: 0.13–0.58, three studies, 844 children, low quality of evidence) compared with control. After adjustment for maternal pre-pregnancy BMI, this association remained in offspring of T1DM, but disappeared in those of GDM mothers. Offspring of GDM mother had higher 2-hour plasma glucose from prepubertal to early adulthood (pooled MD: 0.43 mmol/L, 95% CI: 0.18–0.69, five studies, 890 children), while those of T1DM mothers had higher rate of T2DM in 2–5 years old to early adulthood (pooled odds ratio [OR], 6.10: 95% CI: 1.23–30.37, two studies, 448 children, very low quality of evidence) compared with control. As there was only one study with offspring of T2DM mothers, evidence is sparse.LimitationsOnly observational studies were included, with a few adequately adjusted for covariables.ConclusionsExposure to maternal hyperglycemia was associated with offspring obesity and abnormal glucose tolerance especially in offspring of T1DM mothers, but the evidence relies on observational studies with low quality of evidence only.

Relationships of maternal body mass index and plasma biomarkers with childhood body mass index and adiposity at 6 years: The Children of SCOPE study

“…Similar results have been reported in a cohort of 618 mother and child dyads; the authors found associations between maternal hypertension and offspring risk of overweight or obesity at 4 years of age. Similarly, there are previous reports of an association between maternal GDM and offspring adiposity, although a recent systematic review concluded that the relationship between GDM and offspring BMI z‐score was not evident following adjustment for maternal BMI …”

High glucose alters fetal rat islet transcriptome and induces progeny islet dysfunction

“…Independent of genetic risk, offspring born from diabetic pregnancies experience a greater risk of insulin resistance, pancreatic islet dysfunction and type 2 diabetes (Ratner et al 2008, Fraser & Lawlor 2014, Tam et al 2017, Das Gupta et al 2018. Such risk of transmission is thought to result from maternal hyperglycemia (Kubo et al 2014, Tam et al 2017, Kawasaki et al 2018; however, no direct evidence exists elucidating the exact role of maternal hyperglycemia in programming offspring metabolic health. Our fetomaternal hyperglycemia model, capable of inducing localized maternal and fetal hyperglycemia, addresses this knowledge gap.…”

Physical development of newborns born to mothers with different carbohydrate metabolism disorders

“…Полученные нами данные также можно объяснить общностью генетических механизмов СД-2 и ГСД. Сегодня доказано, что развитие СД является следствием генетической предрасположенности к заболеванию [40][41][42][43][44][45][46][47][48][49][50]. К развитию ГСД и СД-2 причастны полиморфизмы тождественных генов [41][42][43], отвечающих за синтез и секрецию инсулина (INS, KCNJ11, АВСС8, TCF7L2, ND1), связанных с передачей инсулинового сигнала (INSR, IGF2, IRS1), регулирующих углеводный и липидный обмены (PPARG, PPARGC1A, ADRB3, GLUT1, ADIPOQ, FOXC2) и пр.…”