Abstract
Uric acid (UA) levels are associated with many diseases including those related to lifestyle. The aim of this study was to evaluate the influence of clinical and anthropometric parameters on UA and xanthine (X) levels during pregnancy and postpartum in women with physiological pregnancy and pregnancy complicated by gestational diabetes mellitus (GDM), and to evaluate their impact on adverse perinatal outcomes. A total of 143 participants were included. Analyte levels were determined by HPLC with ultraviolet detection (HPLC-UV). Several single-nucleotide polymorphisms (SNPs) in UA transporters were genotyped using commercial assays. UA levels were higher within GDM women with pre-gestational obesity, those in high-risk groups, and those who required insulin during pregnancy. X levels were higher in the GDM group during pregnancy and also postpartum. Positive correlations between UA and X levels with body mass index (BMI) and glycemia levels were found. Gestational age at delivery was negatively correlated with UA and X levels postpartum. Postpartum X levels were significantly higher in women who underwent caesarean sections. Our data support a possible link between increased UA levels and a high-risk GDM subtype. UA levels were higher among women whose glucose tolerance was severely disturbed. Mid-gestational UA and X levels were not linked to adverse perinatal outcomes.
Highlights
Uric acid (UA) is a terminal product of purine metabolism with non-negligible extracellular antioxidant function; increased UA levels are established markers of pathological mechanisms involved in a plethora of diseases [1]
Major findings of the current study can be summarized as follows: (i) UA levels were higher in women with pre-gestational overweight/obesity, in the high-risk group, and in those who required insulin therapy; (ii) UA levels were positively correlated with body mass index (BMI) and glycemia both during pregnancy and postpartum; (iii) gestational age at delivery was negatively correlated with UA levels postpartum; and (iv) the genetic component for UA levels was confirmed for rs1014290, rs12498742, rs734553, and rs16890979 in glucose transporter 9 (GLUT9)
Our data suggest an association of UA levels with impaired glucose tolerance within gestational diabetes mellitus (GDM) women during pregnancy
Summary
Uric acid (UA) is a terminal product of purine metabolism with non-negligible extracellular antioxidant function; increased UA levels are established markers of pathological mechanisms involved in a plethora of diseases [1]. UA production is maintained by an enzyme, xanthine oxidoreductase (XOR), which catalyzes the oxidation from hypoxanthine to xanthine (X) and the subsequent oxidation from X to UA [2]. Long-term hyperuricemia (i.e., levels higher than 360 μmol/L in women and 420 μmol/L in men) typically seen in gout or even short-term elevation associated with tumor lysis syndrome may lead to the formation of urate calculi in kidney and other tissues. Despite its limited solubility and a fate of waste product, UA is largely (~90%) reabsorbed in the kidney and the intestine and returned to the blood. Increased UA levels may occur as a result of an increased UA production, impaired renal UA excretion, or both [3]. Hyperuricemia itself is linked to atherosclerosis and basically to all components of metabolic syndrome such as visceral obesity, hypertension, dyslipidemia, insulin resistance, and diabetes mellitus [4], and several studies showed UA to be one of the hallmarks of the metabolic syndrome [5,6,7,8]
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