Chemerin is highly expressed in the serum, placenta tissue, and umbilical cord blood of diabetic mother; however, the impact of chemerin on cognitive disorders of offspring from mothers with diabetes in pregnancy remains unclear.
Serum adiponectin was lower in women with GDM and GIGT at both 1-year and 3-years (both P ≤ 0.002), whereas chemerin, RBP-4, CRP and PAI-1 showed no differences across the 4 groups.
Our finding showed that the genotypes frequency of chemerinrs4721 polymorphism was significantly different between GDM and non-GDM groups (χ<sup>2</sup> = 7.44, P = 0.02).
There was significant heterogeneity among studies (I<sup>2</sup> = 98.0%, P < 0.001); however, heterogeneity disappeared or markedly decreased in the subgroups of European populations (I<sup>2</sup> = 0.0%, P = 0.531), age ≥ 30 years (I<sup>2</sup> = 28.2%, P = 0.223) and WHO diagnostic criteria (I<sup>2</sup> = 0.0%, P = 0.490) when stratifying by study location, trimester of chemerin measurement and the diagnostic criteria of GDM.
This finding together with the positive association of chemerin and leptin with markers of insulin resistance, suggests that these adipokines and more especially chemerin and leptin accompanied by their adipose tissue expression could contribute to the increased insulin resistance and low grade inflammation that characterizes GDM-obese women.
Non-diabetic women with a history of GDM in a previous pregnancy (n=123) had blood drawn at 14 and 28weeks of pregnancy for GDM diagnosis, together with assessment of a range of adipokine concentrations by multiplex assay (fatty acid-binding protein 4 [FABP4], leptin, chemerin, adiponectin and resistin).