745.1 - Altered Adipose Tissue Inflammatory Markers in Mothers With Gestational Diabetes
Sunday, April 3, 2022
2:15 PM – 2:30 PM
Room: 304 - CC - Pennsylvania Convention Center
Introduction: The Virendra B. Mahesh Award of Excellence in Endocrinology and Metabolism is to promote the career development of young investigators pursuing research in the area of Endocrinology. The award will be presented to an outstanding graduate student or postdoctoral fellow who is a rising star in the field of Endocrinology and Metabolism.
Alan Maloney (University of Missouri), Jillian Barnas (University of Missouri), Victoria Vieira-Potter (University of Missouri), Jill Kanaley (University of Missouri)
Introduction: Adipose tissue (AT) releases adipokines and inflammatory cytokines which may have an impact on the fetus during pregnancy. Mothers with gestational diabetes (GDM) have children who have an increased risk of developing obesity and diabetes compared to children born to normal glucose tolerant (NGT) mothers, but the mechanisms are not known. AT dysfunction in mothers with GDM may play a mechanistic role in the relationship. HYPOTHESIS: Mothers with GDM will have impaired AT mitochondrial function and increased markers of inflammation. Methods: AT tissue samples were collected from 22 NGT and 6 GDM pregnant women undergoing a C-section. Subcutaneous (SQ) and visceral AT (VAT) samples, mothers blood, and fetal cord blood were collected. AT samples were assessed for protein expression (via Western blot) of EGF-like module-containing mucin-like hormone receptor-like 1; estrogen receptors (ERα and ERβ); adiponectin; mitochondrial oxidative phosphorylation (Ox-phos) C1-5; nuclear factor kappa-light-chain-enhancer of activated B cells; adipose triglyceride lipase (ATGL) and a panel of inflammatory, mitochondrial, and metabolic genes via quantitative real time polymerase chain reaction. Mother’s blood and cord blood were assessed for presence of adiponectin, brain derived neurotrophic factor, C-reactive protein. and non-esterified fatty acids via enzyme-linked immunoassay. Results: In GDM compared to NGT mothers, VAT had significantly lower protein expression levels of Ox-phos C2 and adiponectin (p=0.009 and 0.008 respectively) and trended towards significance for ATGL and Ox-phos C3 (p=0.05 and 0.06 respectively). Gene expression of adiponectin and ERβ also tended to be lower in GDM mothers (p=0.05 and 0.06 respectively). In SQAT, higher gene expression of mannose receptor C-type 1 (anti-inflammatory macrophage marker) in the GDM mothers was found (p=0.037). No differences in the measured blood markers were found. Conclusion: Data support that mothers with GDM differentially express AT adipokines and genes associated with inflammation, insulin resistance and altered lipid metabolism than mothers with NGT.
