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Published on: June 3, 2016
Effects of APOA5 S19W polymorphism on growth, insulin sensitivity and lipoproteins in normoweight neonates
Eva Gesteiro1, Sara Bastida, Miguel Vázquez-Velasco
1Servicio de Análisis Clínicos, Hospital de Mérida, Polígono Nueva Ciudad s/n Mérida, Badajoz, Spain.
Insights
The APOA5 S19W polymorphism impacts neonatal growth and metabolism. W allele carriers show lower birth weight and altered insulin/lipoprotein profiles, suggesting suboptimal fetal nutrition and poorer antioxidant status.
Area of Science:
- Genetics and Molecular Biology
- Neonatal Metabolism and Endocrinology
- Lipid Metabolism and Cardiovascular Health
Background:
- Apolipoprotein A5 (ApoA5) is crucial for activating lipoprotein lipase (LPL), a key enzyme in triglyceride-rich lipoprotein metabolism.
- Placental LPL activity influences fetal fat deposition and growth.
- The APOA5 gene harbors common polymorphisms, such as S19W, which may affect metabolic processes.
Purpose of the Study:
- To investigate the association between the APOA5 S19W polymorphism and neonatal anthropometry, lipoprotein levels, hormone concentrations, and insulin sensitivity.
- To explore the impact of this polymorphism on fetal growth and neonatal metabolic parameters in a cohort of Caucasian newborns.
Main Methods:
- Analysis of the APOA5 S19W polymorphism in 58 normal-weight Caucasian newborns from the Mérida cohort.
- Measurement of neonatal anthropometrical parameters (BMI, ponderal index, birth weight).
- Assays for lipoprotein concentrations (Apo B, LDL), oxidized LDL (LDLox), insulin, cortisol, and calculation of HOMA-R and insulin/cortisol ratio.
Main Results:
- Neonates with the W allele exhibited significantly lower BMI, ponderal index, and birth weight compared to S-homozygous newborns.
- W allele carriers displayed lower insulin levels, insulin/cortisol ratio, HOMA-R, and Apo B values, but higher LDLox and LDLox/LDL ratio.
- Maternal-neonatal S19W polymorphism concurrence was linked to impaired fetal growth but did not alter neonatal lipid profiles.
Conclusions:
- The APOA5 S19W polymorphism is associated with altered fetal growth and metabolic regulation in neonates.
- W allele carriers appear to have received suboptimal nutrition during gestation, evidenced by reduced body weight and altered metabolic markers.
- Neonates carrying the W allele demonstrate an inferior lipoprotein antioxidant status compared to their S-homozygous counterparts.
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 < 0.001), ponderal index (P < 0.001), birth weight (P < 0.01), insulin levels (P < 0.05), the insulin/cortisol ratio (P < 0.05), HOMA-R (P < 0.05) and Apo B values (P < 0.01), but higher oxidised LDL (LDLox) values and a higher LDLox/low-density lipoprotein (LDL) ratio (both P < 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.
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Lethal Alleles
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
