The percentage of pregnancies accompanied by gestational diabetes (GDM) is increasing
globally. Also, GDM and the associated disturbances in maternal lipid metabolism are
shown to have negative impacts on maternal and fetal long term health. In normoglycemic
women (NGT), the pancreas can compensate for the reduction in insulin sensitivity
being present in the 3rd trimester of pregnancy. However in GDM, the compensatory beta cell response is absent.
It is proposed that adipokines, also released from the placenta might lead to reduced
compensatory effects of the beta cells.
In our clinical PREG study at the IDM in Tübingen we have access to blood and placenta
samples of well characterized NGT (n = 18) and GDM (n = 8) women. Hypertriglyceridemia,
accumulation of defined free fatty acids and triglycerides in the placenta as well
as increased mRNA levels of proinflammatory cytokines (IL1b, IL6, and IL8) and enzymes
involved in placental lipid metabolism (i.e.: LIPG, CD36, FASN) are detected via GC-analysis
and qRT-PCR in our cohort. This data indicate that GDM and increased maternal BMI
have an influence on the lipid metabolism of the placenta and may lead to a proinflammatory
placental milieu. Also, in the placenta samples we see an increase in apelin mRNA
levels of women with GDM. Apelin is shown to reduce insulin release of the beta cells
via activation of PI3-kinase-phosphodiesterase-3b. In further steps we will determine
protein levels of apelin in placenta of mothers with NGT and GDM, and investigate
a putative epigenetic regulation of apelin in the placenta.