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Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance with first onset or first identification in pregnancy. It is one of the most common complications of pregnancy with a prevalence ranging from 3% to upwards of 16% depending on the screened population and whether a 1 or 2-step screening algorithm is utilized. Its occurrence has historically been predominantly attributed to pro-diabetogenic placental hormone secretion. However, there is emerging evidence to indicate that its mechanistic underpinnings are more complex; similar to type 2 Diabetes Mellitus (T2DM), adipose tissue dysfunction and associated inflammation may be key etiologic factors for the development of GDM. In support of this view, women with a history of GDM are at high risk of subsequent T2DM development and their offspring at increased risk of obesity and metabolic syndrome across their life span. With immediate and long term consequences of GDM on mother and offspring, etiologic understanding that can inform therapeutic and preventative targets is essential. This review article explores the existing literature as it relates to associations of GDM with expansion of adipose tissue depots, secretion of adipose derived biologically active factors, and inflammation and inflammatory related substances.
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Simas et al. (2014) studied this question.
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