Resistin is a secreted protein implicated in the pathogenesis of obesity and type 2 diabetes. It was discovered in rodents as an adipocyte-derived factor which induces insulin resistance (Steppan et al. 2001). Human and murine resistin only share 59% homology at the amino acid level (Ghosh et al. 2003). Unlike rodent resistin, human resistin is predominantly produced by peripheral blood mononuclear cells (PBMCs), macrophages, and bone marrow cells (Schwartz and Lazar 2011). Human resistin has been shown to induce expression of proinflammatory cytokines and adhesion molecules in the settings of inflammation and endothelial dysfunction. Given the strong relationship between inflammation and metabolism, there is mounting evidence suggesting a role for human resistin in the pathological processes of metabolic diseases, including obesity, diabetes, and cardiovascular diseases (Lazar 2007; McTernan et al. 2002). However, the precise mechanism by which resistin impacts these processes has not been clearly defined as several studies have failed to identify an association of resistin levels with obesity or type 2 diabetes (Gerber et al. 2005; Pfutzner et al. 2003). Resistin has been implicated in the insulin resistance observed in normal pregnancy, as the level of resistin increases with gestational age and decreases after delivery (Chen et al. 2005). Conflicting evidence exists regarding the association of maternal resistin levels with GDM. Recent meta-analysis suggests GDM is associated with increased maternal resistin levels (Hu et al. 2019), while resutls of another meta-analysis do not indicate a significant change of resitin levels in gestational diabetes (Bellos et al. 2019). Available prospective data are also inconsistent regarding the link of maternal resistin to the later development of GDM (Bao et al. 2015). Much less is known about fetal resistin levels and current studies examining the fetal levels of resistin in diabetes during pregnancy are inconsistent (Shang et al. 2018; Oncul et al. 2013; Mohamed et al. 2010). The aims of the present study are to assess the regulation and function of human resistin in fetal circulation and how it affects placenta in diabetes during pregnancy.