Placental expression of lipoprotein lipase (LPL), endothelial lipase (EL) and hormone sensitive lipase (HSL) in pregnancies complicated by gestational diabetes mellitus (GDM) (#203)
Background
Infants of women with GDM have a greater risk of macrosomia and a greater percentage body fat even with good maternal glycaemic control (1), which may be caused by elevated maternal lipids (2). Placental lipases such as LPL, EL and HSL transfer lipids (3). Previous studies of LPL and EL expression in placentae in women with GDM have reported divergent results possibly due to differences in maternal obesity and gestational age (4-6). The expression of HSL has not been examined in GDM. The purpose of this study was to examine the expression of LPL, EL and HSL in term pregnancies complicated by GDM.
Subjects
Placentae from 9 women with GDM and 12 normoglycaemic pregnancies, matched for maternal BMI and gestational age of delivery were collected with informed consent at the RBWH.
Methods
RNA was extracted and reverse transcribed. Gene expression levels for LPL, EL and HSL were determined with real time PCR and analysed with the ΔΔCt method. For standardisation of tissue composition, the lipase expression was normalised to expression of ß-actin. Desmin (smooth muscle cells), Cytokeratin 7 (trophoblasts) and CD34 (endothelial cells) were assessed to determine tissue composition. Data were analysed using Mann-Whitney U tests.
Results
There was no difference in maternal BMI (GDM: 32.6±10.8 kg/m2 (mean±SD) vs 29.0±8.0 kg/m2) or gestational age of delivery (GDM: 38.6±0.8 weeks vs 38.0±0.9 weeks). HSL expression was reduced in placentae from GDM (GDM: 0.65±0.43 vs control 1.15±0.65, P =0.03). There was no difference in expression of LPL or EL between GDM and normoglycaemic placentae.
Conclusions
These results suggest that GDM is associated with decreased expression of HSL in placenta. Decreased expression of the intracellular lipase HSL may reflect reduced lipase activity due to inhibition by insulin. These results need to be confirmed with an increased sample size and analysis of HSL protein levels and/or activity.
- Schaefer-Graf UM, Graf K, et al. Diabetes Care. 2008 Sep;31(9):1858-63.
- Herrera E, Ortega-Senovilla H. Best Pract Res Clin Endocrinol Metab. 2010 Aug;24(4):515-25.
- Gauster M, Desoye G, et. al., Diabetes Mellitus. Curr Diab Rep. 2011 Nov 19.
- Gauster M, Hiden U, et.al., Diabetes. 2011 Oct;60(10):2457-64.
- Lindegaard ML, Damm P, et.al., J Lipid Res. 2006 Nov;47(11):2581-8.
- Magnusson AL, Waterman IJ, et.al., J Clin Endocrinol Metab. 2004 Sep;89(9):4607-14.