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.
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).
In this sense, 1st-2nd trimester-released biomarkers found in maternal plasma including adipose tissue-derived factors such as adiponectin, visfatin, omentin-1, fatty acid-binding protein-4 and retinol binding-protein-4 have shown correlations with GDM development.
The aim of this study was to investigate the correlations and interactions between the polymorphisms of insulin resistance-related genes (ADIPOQrs2241766), inflammation factors (TNF-α rs1800629, IL-6 rs1800795), obesity-related genes (GNB3 rs5443, ADRB rs1042714), and risk factors for gestational diabetes mellitus (GDM) such as diet structure in the development of 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.
Secondly, maternal obesity (in the absence of gestational diabetes) was associated with (i) elevated DNA methylation of the leptin promoter on fetal side only, (ii) hypomethylation of the adiponectin promoter on the maternal side only, (iii) significantly low levels of leptin receptor protein (albeit in the absence of differences in mRNA levels and promoter DNA methylation), (iv) significantly low levels of adiponectin receptor 1 mRNA expression on the maternal side only, and (v) elevated DNA methylation of the adiponectin receptor 2 promoter on the maternal side only.
Maternal GDM increased adipose mRNA levels of peroxisome proliferator-activated receptor gamma (Pparg) and adiponectin (Adipoq) in 31-week-old CD-fed male offspring, and increased mRNA levels of insulin receptor (Insr) and lipoprotein lipase (Lpl) in 31-week-old male offspring on both diets.
Insulin, HOMA-IR, and adiponectin levels mediated the WHR-GDM association by 9% to 11%; corresponding mediation proportions for the WC-GDM association were 35% to 41% (all P < 0.04).
Elevated leptin and decreased adiponectin concentrations associated with adverse metabolic traits and were most likely driven by higher obesity prevalence among GDM offspring.
Serum adiponectin was negatively correlated with maternal age and HOMA-IR in the NP group (p < 0.05 all) and with placental weight and serum omentin in the GDM group (p < 0.05 all).
HMW adiponectin did not improve prediction of IADPSG GDM (AUC 0.84, sensitivity 64%, specificity 97.9%, P = 0.22) compared to FG and maternal factors (0.79, 56%, 93.8%).
Our findings suggest that omentin-1, rather than adiponectin, could be useful as a predictor of preterm birth in patients with gestational diabetes mellitus.
Adiposity, low hip circumference, serum biomarkers (increased level of alanine aminotransferase, gamma-glutamyl transferase, uric acid and C-reactive protein, and decreased level of adiponectin and vitamin D), an unhealthy dietary pattern (increased consumption of processed meat and sugar-sweetened beverages, decreased intake of whole grains, coffee and heme iron, and low adherence to a healthy dietary pattern), low level of education and conscientiousness, decreased physical activity, high sedentary time and duration of television watching, low alcohol drinking, smoking, air pollution, and some medical conditions (high systolic blood pressure, late menarche age, gestational diabetes, metabolic syndrome, preterm birth) presented robust evidence for increased risk of T2DM.
Our aim was to study the expression of adipokine-encoding genes (leptin, adiponectin, and angiopoietin-like protein 4 (ANGPTL4)) in human umbilical vein endothelial cells (HUVECs) and adipokine concentration in cord blood from women with gestational diabetes mellitus (GDM) depending on glycaemic targets.
The expression of adipokines, leptin, and resistin were significantly increased, but adiponectin was decreased in OATs from patients with GDM compared with those without GDM.
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.
The ratio of ficolin-3/adiponectin at 16-18 weeks of gestation was changed in pregnant women who subsequently developed GDM, and might provide effective early predicting and screening for GDM.
Pearson's correlation analysis of adiponectin and resistin in all the subjects with various GDM risk factors showed a negative association of adiponectin (r = -0.32, p = .05) and a positive correlation of resistin (r = 0.41, p = .01) with LDL cholesterol.
Among the four hormones, adiponectin was inversely associated with infant growth in both the GDM (β weight-for-height=-2·49; 95 % CI -3·83, -1·15; P<0·001; β head-circumference=-0·39; 95 % CI -0·65, -0·13; P=0·003) and healthy groups (β weight-for-height=-1·42; 95 % CI -2·38, -0·46; P=0·003; β head-circumference=-0·15; 95 % CI -0·27, -0·03; P=0·007).