Metabolic dysfunction is exacerbated in visceral, not subcutaneous, adipose tissue in gestational diabetes.

Adipose tissue (AT) releases adipokines and inflammatory cytokines, which may have an adverse impact on the mother and fetus during pregnancy. Mothers with gestational diabetes mellitus (GDM) differentially express adipokines and cytokines compared to normal glucose tolerant (NGT) mothers, but the mechanisms are unknown. The purpose of this study was to identify molecular mechanisms in subcutaneous (SQAT) and visceral AT (VAT) which may help characterize GDM and pinpoint those that contribute to its pathology. SQAT and VAT samples were collected from 22 NGT and six GDM pregnant women undergoing a C-section. A panel of inflammatory, mitochondrial, and metabolic genes and proteins (via q-rtPCR and Western blot) was measured. Blood was assessed for concentrations of adiponectin, brain neurotrophic factor, C-reactive protein, and non-esterified fatty acids (via ELISA). In GDM, VAT protein content was lower for oxidative phosphorylation complexes CI-CIII, adiponectin, and adipose triglyceride lipase. Gene expression of adiponectin, estrogen receptor β, uncoupling protein 1, and peroxisome proliferator-activated receptor gamma was also lower in GDM mothers, while gene expression of an anti-inflammatory macrophage marker was higher. No differences in the measured blood markers were found. Mothers with GDM differentially express AT adipokines and genes associated with inflammation, insulin resistance, and altered lipid metabolism relative to mothers with NGT.