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Increased Lipoprotein associated phospholipase A 2  (LpPLA 2 ) has been associated with inflammatory pathologies, including Type 2 Diabetes. Studies on LpPLA 2  and Gestational Diabetes Mellitus (GDM) are rare, and have focused mostly on maternal outcome. In the present study, we investigated whether LpPLA 2  activity on foetal lipoproteins is altered by maternal GDM and/or obesity (a major risk factor for GDM), thereby contributing to changes in lipoprotein functionality. We identified HDL as the major carrier of LpPLA 2  activity in the foetus, which is in contrast to adults. We observed marked expression of LpPLA 2  in placental macrophages (Hofbauer cells; HBCs) and found that LpPLA 2  activity in these cells was increased by insulin, leptin, and pro-inflammatory cytokines. These regulators were also increased in plasma of children born from GDM pregnancies. Our results suggest that insulin, leptin, and pro-inflammatory cytokines are positive regulators of LpPLA 2  activity in the foeto-placental unit. Of particular interest, functional assays using a specific LpPLA 2  inhibitor suggest that high-density lipoprotein (HDL)-associated LpPLA 2  exerts anti-oxidative, athero-protective functions on placental endothelium and foetus. Our results therefore raise the possibility that foetal HDL-associated LpPLA 2  might act as an anti-inflammatory enzyme improving vascular barrier function.

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Maternal Gestational Diabetes Mellitus increases placental and foetal lipoprotein-associated Phospholipase A2 which might exert protective functions against oxidative stress