Skip to main content
ARS Home » Northeast Area » Boston, Massachusetts » Research » Publications at this Location » Publication #284776

Title: Effects of APOA5 S19W polymorphism on growth, insulin sensitivity and lipoproteins in normoweight neonates

Author
item GESTEIRO, EVA - The Hospital Of Merida
item BASTIDA, SARA - Complutense University Of Madrid (UCM)
item VAZQUEZ-VALASCO, MIGUEL - Complutense University Of Madrid (UCM)
item CORELLA, DOLORES - University Of Valencia
item GUILLEN, MARISA - University Of Valencia
item ORDOVAS, JOSE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item SANCHEZ-MUNIZ, FRANCISCO - Complutense University Of Madrid (UCM)

Submitted to: European Journal of Pediatrics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/4/2011
Publication Date: 12/1/2011
Citation: Gesteiro, E., Bastida, S., Vazquez-Valasco, M., Corella, D., Guillen, M., Ordovas, J.M., Sanchez-Muniz, F.J. 2011. Effects of APOA5 S19W polymorphism on growth, insulin sensitivity and lipoproteins in normoweight neonates. European Journal of Pediatrics. 170(12):1551-1558.

Interpretive Summary: Apolipoprotein (Apo) A5 is a protein involved in the activation of lipoprotein lipase (LPL) and the metabolism of triglyceride (TG)-rich lipoproteins. LPL plays a major role in the metabolism of TG-rich lipoproteins, and placental LPL activity is known to correlate positively with foetal fat deposition and size. Moreover, it is well known that early metabolic events in life are associated with health later in life. Therefore, we examined the association between a common APOA5 S19W polymorphism and neonatal anthropometrical measurements, lipoprotein and hormone concentrations, and insulin sensitivity in 58 normal weight Caucasian newborns. Neonates with the W allele displayed lower BMI, ponderal index, birth weight, insulin levels, insulin/cortisol ratio, HOMA-R and Apo B values, but higher oxidized LDL (LDLox) values and a higher LDLox/low-density lipoprotein (LDL) ratio than S-homozygous newborns. The APOA5 S19W polymorphism was associated with foetal growth as well as with glucose and lipoprotein metabolism in the neonates. In conclusion, these findings suggest that the W allele carriers received a less optimal nutrition during gestation and that their lipoprotein antioxidant status was inferior to that of their homozygous S allele counterparts and this can put them at risk for metabolic disorders later in life.

Technical Abstract: Apolipoprotein (Apo) A5 is a protein involved in the activation of lipoprotein lipase (LPL) and the metabolism of triglyceride (TG)-rich lipoproteins. LPL plays a major role in the metabolism of TG-rich lipoproteins, and placental LPL activity is known to correlate positively with foetal fat deposition and size. We examine the association between the common APOA5 S19W polymorphism and neonatal anthropometrical measurements, lipoprotein and hormone concentrations, and insulin sensitivity in 58 normal weight Caucasian newborns from the Mérida cohort. Neonates with the W allele displayed lower BMI (P' less than '0.001), ponderal index (P' less than '0.001), birth weight (P' less than '0.01), insulin levels (P' less than '0.05), the insulin/cortisol ratio (P' less than '0.05), HOMA-R (P' less than '0.05) and Apo B values (P' less than '0.01), but higher oxidised LDL (LDLox) values and a higher LDLox/low-density lipoprotein (LDL) ratio (both P' less than '0.05) than S-homozygous newborns. The APOA5 S19W polymorphism was associated with foetal growth as well as with glucose and lipoprotein metabolism in the neonates. Concurrence of the S19W polymorphism in neonates and their mothers did not affect neonatal lipid and lipoprotein concentrations but was associated with impaired foetal growth. Specifically, W allele carriers displayed a higher degree of LDL oxidation and lower body weight, plasma insulin values, insulin/cortisol ratio and Apo B concentrations than homozygotes for the common S allele. In conclusion, these findings suggest that the W allele carriers received a less optimal nutrition during gestation and that their lipoprotein antioxidant status was inferior to that of their homozygous S allele counterparts.