Cord-blood lipoproteins, homocysteine, insulin sensitivity/resistance marker profile, and concurrence of dysglycaemia and dyslipaemia in full-term neonates of the Mérida Study

Abstract

Early alterations in glucose homeostasis increase the risk of developing insulin resistance and obesity later in life. The concurrence of altered lipids and insulin sensitivity/resistance markers at birth has been scarcely investigated. The study aimed to ascertain level ranges of homocysteine (tHcyt), arylesterase (AE), lipids/lipoproteins, and insulin resistance/sensitivity markers in full-term neonates and to determine the concurrence effect of dyslipaemia and dysglycaemia on those parameters at birth. Participants were 197 full-term, 2.5 to <4.0 kg, without foetal distress Spanish newborns from the Mérida Study. Parameter percentiles for males and females were stated. The effect of the concurrence high glucose/high triglycerides (high glucose/high TG) or high glucose/low cholesterol transported by HDL (HDL-c) on tHcyt, LDL-c, HDL-c, lipoprotein (a) (Lp(a)), oxidised LDL (oxLDL), AE, glucose, insulin sensitivity (QUICKI) and insulin resistance index (HOMA-IR) was studied. Females had higher total cholesterol (TC), HDL-c, Apo A1, Lp(a) and HDL-c/Apo A1, but lower relative transport of TC (%TC) by the very low lipoprotein fraction than males. No gender differences were found for glucose, HOMA-IR and QUICKI. Neonates at the 2.5- to 2.999-kg range display more adequate HOMA-IR and QUICKI levels that their >3.0 kg counterparts. The concurrence of high glucose/high TG or high glucose/low HDL-c increased TC/HDL-c and HOMA-IR, but decreased, oxLDL, oxLDL/LDL-c and QUICKI with respect to that of low glucose/low TG or glucose/high HDL-c. The concurrence glucose/TG has predictive value for low QUICKI, whilst that of glucose/HDL-c for low QUICKI and high HOMA-IR, suggesting the importance of routine TG, HDL-c and glucose screening at birth as it would identify candidates for insulin resistance.