Diabetes and Pregnancy

Feig, Denice S.; Berger, Howard; Donovan, Lois; Godbout, Ariane; Kader, Tina; Keely, Erin; Sanghera, Rema

doi:10.1016/j.jcjd.2017.10.038

Cited by 240 publications

(190 citation statements)

References 471 publications

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“…It is widely recommended that women with recent GDM undergo glucose screening within the first 6 months after delivery . Whereas the incidence of overt diabetes in the early postpartum period is generally not high (ostensibly reflecting pre‐existing type 2 diabetes that was first identified in pregnancy and hence diagnosed as GDM), the prevalence of prediabetes in this population is considerable, with approximately 30% of women with GDM exhibiting impaired glucose tolerance at 3 months after delivery .…”

Section: Management Of Maternal History Of Gestational Diabetes Mellitusmentioning

confidence: 99%

FIGO (International Federation of Gynecology and Obstetrics) Postpregnancy Initiative: Long‐term Maternal Implications of Pregnancy Complications—Follow‐up Considerations

Sheiner

Kapur

Retnakaran

et al. 2019

Intl J Gynecology & Obste

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Section: Management Of Maternal History Of Gestational Diabetes Mellitusmentioning

confidence: 99%

FIGO (International Federation of Gynecology and Obstetrics) Postpregnancy Initiative: Long‐term Maternal Implications of Pregnancy Complications—Follow‐up Considerations

Sheiner

Kapur

Retnakaran

et al. 2019

Intl J Gynecology & Obste

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“…Between 3 and 20% of women develop GDM, depending on their risk factors (Feig et al . ). GDM increases the risk of the mother developing subsequent type 2 diabetes mellitus (T2DM) by up to 7‐fold compared to euglycaemic pregnancies (Melchior et al .…”

Section: Introductionmentioning

confidence: 97%

A mouse model of gestational glucose intolerance through exposure to a low protein diet during fetal and neonatal development

Szlapinski

King

Retta

et al. 2019

The Journal of Physiology

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Key points Pancreatic β‐cell dysfunction is hypothesized to be the significant determinant of gestational diabetes pathogenesis, however pancreatic samples from patients are scarce. This study reports a novel mouse model of gestational glucose intolerance in pregnancy, originating from previous nutrition restriction in utero, in which glucose intolerance was restricted to late gestation as is seen in human gestational diabetes. Glucose intolerance was attributed to reduced β‐cell proliferation, leading to impaired gestational β‐cell mass expansion in maternal endocrine pancreas, in addition to reduced glucose‐stimulated insulin secretion. This model reproduces some of the features of gestational diabetes and is suitable for testing safe therapeutic interventions that increase β‐cell mass during pregnancy and prevent or reverse gestational glucose intolerance. Abstract Gestational diabetes mellitus (GDM) is an increasingly prevalent form of diabetes that appears during pregnancy. Pathological studies link a failure to adaptively increase maternal pancreatic β‐cell mass (BCM) in pregnancy to GDM. Due to the scarcity of pancreatic samples from GDM patients, we sought to develop a novel mouse model for impaired gestational glucose tolerance. Mature female C57Bl/6 mouse offspring (F1) born to dams fed either a control (C) or low‐protein (LP) diet during gestation and lactation were randomly allocated into two subsequent study groups: pregnant (CP, LPP) or non‐pregnant (CNP, LPNP). Glucose tolerance tests were performed at gestational day (GD) 9, 12 and 18. Subsequently, pancreata were removed for fluorescence immunohistochemistry to assess α‐cell mass (ACM), BCM and β‐cell proliferation. An additional group of animals was used to measure insulin secretion from isolated islets at GD18. LPP females displayed glucose intolerance compared to CP females at GD18 (P < 0.001). BCM increased threefold at GD18 in CP females. However, LPP females had reduced BCM expansion (P < 0.01) concurrent with reduced β‐cell proliferation at GD12 (P < 0.05). LPP females also had reduced ACM expansion at GD18 (P < 0.01). LPP islets had impaired glucose‐stimulated insulin secretion in vitro compared to CP islets (P < 0.01). Therefore, impaired glucose tolerance during pregnancy is associated with a failure to adequately adapt BCM, as a result of reduced β‐cell proliferation, in addition to lower glucose‐stimulated insulin secretion. This model could be used to evaluate novel interventions during pregnancy to increase BCM or function as a strategy to prevent/reverse GDM.

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“…Theoretically, limiting maternal intrapartum hyperglycaemia reduces the risk of neonatal hypoglycaemia by preventing an acute rise in fetal insulin secretion before birth. The Joint British Diabetes Societies, National Institute for Health and Clinical Excellence and Canadian guidelines recommend tight intrapartum glucose targets (4.0–7.0 mmol/l) during labour and delivery . However, there are insufficient high quality data confirming an association between maternal intrapartum glucose control and neonatal hypoglycaemia.…”

Section: Introductionmentioning

confidence: 99%

Maternal glycaemic control and risk of neonatal hypoglycaemia in Type 1 diabetes pregnancy: a secondary analysis of the CONCEPTT trial

et al. 2019

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Aims To examine the relationship between maternal glycaemic control and risk of neonatal hypoglycaemia using conventional and continuous glucose monitoring metrics in the Continuous Glucose Monitoring in Type 1 Diabetes Pregnancy Trial (CONCEPTT) participants. Methods A secondary analysis of CONCEPTT involving 225 pregnant women and their liveborn infants. Antenatal glycaemia was assessed at 12, 24 and 34 weeks gestation. Intrapartum glycaemia was assessed by continuous glucose monitoring measures 24 hours prior to delivery. The primary outcome was neonatal hypoglycaemia defined as glucose concentration < 2.6 mmol/l and requiring intravenous dextrose. Results Neonatal hypoglycaemia occurred in 57/225 (25.3%) infants, 21 (15%) term and 36 (40%) preterm neonates. During the second and third trimesters, mothers of infants with neonatal hypoglycaemia had higher HbA1c [48 ± 7 (6.6 ± 0.6) vs. 45 ± 7 (6.2 ± 0.6); P = 0.0009 and 50 ± 7 (6.7 ± 0.6) vs. 46 ± 7 (6.3 ± 0.6); P = 0.0001] and lower continuous glucose monitoring time‐in‐range (46% vs. 53%; P = 0.004 and 60% vs. 66%; P = 0.03). Neonates with hypoglycaemia had higher cord blood C‐peptide concentrations [1416 (834, 2757) vs. 662 (417, 1086) pmol/l; P < 0.00001], birthweight > 97.7th centile (63% vs. 34%; P < 0.0001) and skinfold thickness (P ≤ 0.02). Intrapartum continuous glucose monitoring was available for 33 participants, with no differences between mothers of neonates with and without hypoglycaemia. Conclusions Modest increments in continuous glucose monitoring time‐in‐target (5–7% increase) during the second and third trimesters are associated with reduced risk for neonatal hypoglycaemia. While more intrapartum continuous glucose monitoring data are needed, the higher birthweight and skinfold measures associated with neonatal hypoglycaemia suggest that risk is related to fetal hyperinsulinemia preceding the immediate intrapartum period.

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Diabetes and Pregnancy

Cited by 240 publications

References 471 publications

FIGO (International Federation of Gynecology and Obstetrics) Postpregnancy Initiative: Long‐term Maternal Implications of Pregnancy Complications—Follow‐up Considerations

FIGO (International Federation of Gynecology and Obstetrics) Postpregnancy Initiative: Long‐term Maternal Implications of Pregnancy Complications—Follow‐up Considerations

A mouse model of gestational glucose intolerance through exposure to a low protein diet during fetal and neonatal development

Maternal glycaemic control and risk of neonatal hypoglycaemia in Type 1 diabetes pregnancy: a secondary analysis of the CONCEPTT trial

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