Abstract
Fetuses exposed to gestational diabetes mellitus (GDM) have a higher risk of abnormal glucose homeostasis in later life. The molecular mechanisms of this phenomenon are still not fully understood. Fatty acid binding protein 4 (FABP4) appears to be one of the most probable candidates involved in the pathophysiology of GDM. The main aim of the study was to investigate whether umbilical cord serum FABP4 concentrations are altered in term neonates born to GDM mothers. Two groups of subjects were selected—28 healthy controls and 26 patients with GDM. FABP4, leptin, and ghrelin concentrations in the umbilical cord serum, maternal serum, and maternal urine were determined via an enzyme-linked immunosorbent assay. The umbilical cord serum FABP4 levels were higher in the GDM offspring and were directly associated with the maternal serum FABP4 and leptin levels, as well as the prepregnancy body mass index (BMI) and the BMI at and after delivery; however, they correlated negatively with birth weight and lipid parameters. In the multiple linear regression models, the umbilical cord serum FABP4 concentrations depended positively on the maternal serum FABP4 and negatively on the umbilical cord serum ghrelin levels and the high-density lipoprotein cholesterol. There are many maternal variables that can affect the level of FABP4 in the umbilical cord serum, thus, their evaluation requires further investigation.
Highlights
The association between early life insults in utero and an increased risk of developing certain noncommunicable diseases in later life has been well established [1,2,3]
We found that the maternal serum Fatty acid binding protein 4 (FABP4) levels were significantly the highest in the gestational diabetes mellitus (GDM) patients in the early puerperium in comparison with both the controls and mothers who were characterized by excessive gestational weight gain [18]
Our study revealed that the umbilical cord serum FABP4 levels were significantly higher in the children of the GDM mothers
Summary
The association between early life insults in utero and an increased risk of developing certain noncommunicable diseases in later life has been well established [1,2,3]. Disturbances in the metabolism of carbohydrates and in lipids, which have been observed in newborns of women with diabetes, may influence their metabolic profile later in life [5,6]. In women with additional metabolic stress, such as those with GDM and pre-existing obesity, there are alterations in the glucose and lipid metabolism of the adipose tissue consistent with an increased insulin resistance, leading to an increase in the circulating concentrations of fatty acids and lipids [7,8]. The molecular mechanisms by which intrauterine exposure to hyperglycemia contributes to the development of obesity and diabetes in the future life of that offspring are still awaiting explanation
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