Idit Ron, Ragad Mdah, Roni Zemet, Rakefet Yoeli Ulman, Moran Rathaus, Benny Brandt, Shali Mazaki‐Tovi, Rina Hemi, Ehud Barhod, Amir Tirosh

Adipose tissue‐derived FABP4 mediates glucagon‐stimulated hepatic glucose production in gestational diabetes

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine
Save to CiteDrive Show PDF

AbstractAimsOne of the most common complications of pregnancy is gestational diabetes mellitus (GDM), which may result in significant health threats of the mother, fetus and the newborn. Fatty acid‐binding protein 4 (FABP4) is an adipokine that regulates glucose homeostasis by promoting glucose production and liver insulin resistance in mouse models. FABP4 levels are increased in GDM and correlates with maternal indices of insulin resistance, with a rapid decline post‐partum. We therefore aimed to determine the tissue origin of elevated circulating FABP4 levels in GDM and to assess its potential contribution in promoting glucagon‐induced hepatic glucose production.Materials and MethodsFABP4 protein and gene expression was determined in biopsies from placenta, subcutaneous (sWAT) and visceral (vWAT) white adipose tissues from GDM and normoglycaemic pregnant women. FABP4 differential contribution in glucagon‐stimulated hepatic glucose production was tested in conditioned media before and after its immune clearance.ResultsWe showed that FABP4 is expressed in placenta, sWAT and vWAT of pregnant women at term, with a significant increase in its secretion from vWAT of women with GDM compared with normoglycaemic pregnant women. Neutralizing FABP4 from both normoglycaemic pregnant women and GDM vWAT secretome, resulted in a decrease in glucagon‐stimulated hepatic glucose production.ConclusionsThis study provides new insights into the role of adipose tissue‐derived FABP4 in GDM, highlighting this adipokine, as a potential co‐activator of glucagon‐stimulated hepatic glucose production during pregnancy.

Need a simple solution for managing your BibTeX entries? Explore CiteDrive!

  • Web-based, modern reference management
  • Collaborate and share with fellow researchers
  • Integration with Overleaf
  • Comprehensive BibTeX/BibLaTeX support
  • Save articles and websites directly from your browser
  • Search for new articles from a database of tens of millions of references
Try out CiteDrive

More from our Archive