Lipid dysfunction and adrenomedullin expression in omental versus subcutaneous adipose tissues in diabetic pregnancies

Gestational diabetes mellitus (GDM) is one of the most common complications of pregnancy but the underlying mechanism remains obscure. The aims of this study are to examine if omental adipose tissue (OMAT) and subcutaneous AT (SCAT) differentially express proinflammatory and lipid metabolic adipokines, and if so, whether their regional differences have implications on lipid metabolism in GDM. Paired samples of OMAT and SCAT were excised from pregnant women in scheduled Cesarean sections with non-obese (NOBS), obese (OBS) and GDM. The results showed that the mRNA of monocyte chemoattractant protein (MCP)-1, macrophage marker CD68, and cytokines IL-6, IL-8, and TNF-alpha are increased in OMAT from GDM women compared to that in NOBS and OBS women (P<0.05). Glucose and TNF-alpha dose-dependently enhanced ADM and its receptor components CRLR and RAMPs in human adipocytes. Immunofluorescence showed that ADM and its receptor components are higher in OMAT from GDM women compared to non-GDM women. Further, basal lipolysis was greater in OMAT than in SCAT and ADM stimulates further glycerol release in OMAT, but not in SCAT, and these increases are reduced by ADM antagonist, ADM22-52. We therefore conclude that elevated ADM and its receptor expressions by OMAT, but not by SCAT appear to contribute to the lipid dysregulation in GDM women, and manipulation of ADM may represent one of the novel approaches in minimizing the risk of GDM-related fetal overgrowth.

Automated summary

This study found that certain inflammatory factors and lipid metabolic adipokines in the omental adipose tissue (OMAT) of women with gestational diabetes mellitus (GDM) were increased. The expression levels of adrenomedullin (ADM) and its receptors were also higher in OMAT of GDM women. In addition, basal lipolysis was higher in OMAT and ADM stimulated further glycerol release in OMAT. These findings suggest that the elevated expression of ADM and its receptors in OMAT may contribute to lipid metabolism dysregulation in GDM women.