Abstract

Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist—including insulin and lifestyle interventions—there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.

Keywords

Gestational diabetesMedicineDiabetes mellitusOverweightInsulin resistanceType 2 diabetesObesityPregnancyDiseaseType 2 Diabetes MellitusObstetricsIntensive care medicineInternal medicineEndocrinologyGestation

MeSH Terms

AdiponectinAdipose TissueAnimalsDiabetesGestationalFemaleGlucoseHumansInsulin ResistanceInsulin-Secreting CellsLeptinOxidative StressPregnancyRisk Factors

Affiliated Institutions

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Publication Info

Year
2018
Type
review
Volume
19
Issue
11
Pages
3342-3342
Citations
1563
Access
Closed

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

1563
OpenAlex
97
Influential
1304
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Cite This

Jasmine F. Plows, Joanna L. Stanley, Philip N. Baker et al. (2018). The Pathophysiology of Gestational Diabetes Mellitus. International Journal of Molecular Sciences , 19 (11) , 3342-3342. https://doi.org/10.3390/ijms19113342

Identifiers

DOI
10.3390/ijms19113342
PMID
30373146
PMCID
PMC6274679

Data Quality

Data completeness: 86%