And larger and more rigorous researches were needed to further explore the association of LEP and LEPR gene polymorphisms and GDM among Chinese population.
The aim of this study was to investigate SNPs rs8050136, rs9939609, and rs1421085 of the FTO gene in women with GDM and their associations with maternal pre-pregnancy weight and body mass index, gestational weight gain and mediators of insulin resistance in GDM like leptin, adiponectin, ghrelin and tumor necrosis factor-alpha (TNF-alpha), compared with healthy pregnant controls.
We investigated the association of the polymorphisms rs7799039 (LEP) and rs13266634 (SLC30A8) in a case-control study in Euro-Brazilians with gestational diabetes (GDM, N = 134) and healthy pregnant women (control, N = 180).
Participants in the lowest tertile for leptin and SLeptinR had a 2.8-fold (95% CI 1.0-7.6) and a 5.7-fold (95% CI 1.9-17.3) higher risk of developing GDM compared with the highest tertile, respectively.
The aim of the current clinical trial study was to explore the effects of ALA supplementation on maternal circulating values of adiponectin (A), leptin (L); and A/L, L/A, adiponectin/homeostatic model assessment for insulin resistance (A/H), and malondialdehyde/total antioxidant capacity (MDA/TAC) ratios in pregnant women with gestational diabetes mellitus (GDM).
Plasma leptin and adiponectin concentrations were measured in 160 women at approximately 12 weeks following pregnancy with GDM and compared with infant weight for length z-score at 1 year of age after adjustment for maternal and infant demographic variables.
Cross-sectional analysis of 236 participants in the PPSDiab Study (cohort study of women 3-16 months after delivery, 152 after gestational diabetes (pGDM), 84 after normoglycemic pregnancy (control subjects); consecutively recruited 2011-16); medical history, physical examination with bioelectrical impedance analysis (BIA), whole body magnetic resonance imaging (MRI) (n = 154), 5-point oral glucose tolerance test, cardiopulmonary exercise testing, clinical chemistry including fasting plasma leptin; statistical analysis with Mann-Whitney U and t -test, Spearman correlation coefficient, multiple linear regression.
The aim of the study was to examine the relationships between GDM, cardiovascular risk, and plasma adiponectin, leptin and the leptin/adiponectin (L/A) ratio in pregnancy and at 5 years after the index pregnancy.
GO terms relevant to translation and metabolic process and their related genes CREB1, ribosomal proteins and LEP, still the inflammation-related proteins (e.g., IGF1 and CALM1) and cell adhesion-related protein FN1 may work together and be essential for GDM.
Using a structural equations model, we observed that gestational diabetes mellitus is a mediator of the effects of prepregnancy obesity on placental leptin DNA methylation (β = 0.81, 95% confidence interval, 0.27-2.71).
This review focuses on the pathophysiology of insulin and adenosine receptors and l-arginine and adenosine membranes transporters giving an overview of the key adipokines leptin and adiponectin in the foetoplacental vasculature in GDM.
Leptin, progesterone, estradiol estimated in this study were increased in the gestational diabetes mellitus women and fairly predicted gestational diabetes in the non-diabetics pregnant women.
After adjustment for confounders including maternal pre-pregnancy BMI, GDM offspring had borderline higher leptin (p=0.06) and significantly lower FGF21 concentrations (p=0.006).
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).
Our results provide evidence that leptin administration during late gestation can reduce adiposity and improve glucose tolerance in the db/+ mouse model of spontaneous GDM.