Endocrine Abstracts (2007) 14 P267

The polymorphism of PPAR and susceptibility to atherosclerosis in children with low birth weight (below 2500 g)

Ewa Barg, Anna Skoczynska, Beata Wikiera, Dorota Chacka, Ewa Glab, Arleta Lebioda & Barbara Turczyn

Wroclaw Medical University, Wroclaw, Poland.

Children, who are born with low birth weight (less 2500 g) are known to have an increased risk of developing lipid disturbances and atherosclerosis in later live.

PPAR alpha activity could play a regulatory role in the pathogenesis of hyperlipidemia and a modulatory role in the control of inflammatory response.

The aim of this study was to determine whether the presence of polymorphism in gene of peroxisome proliferators-activated receptor(PPAR) alpha is associated with lipid disturbances and susceptibility to apoptosis in children with low birth weight.

Methods: The associations between L162V polymorphism in the gene for PPAR alpha and

lipid peroxidation, lipid profile, activity of caspase3 and apoptosis activation was examined in 155 children with low birth weight aged 4–11 years, and in 30 children born with normal weight as a control group.

Results: The frequency of the V allele of the L162 polymorphism gene in PPAR alpha gene in children(0.07) was similar to that in general population(0.06 in controls).

In the group with polymorphism gene 4 children with LBW have the 50 Kb domain on the DNA electrophoretic profiles, but 7 children with LBW and control children haven’t it.

The effect of the l162V polymorphism within PPAR alpha gene on the serum total HDL levels are observed (P<0.001).The levels of HDL and triglycerides and lipid peroxides were statistically higher in children with gene PPAR polymorphism (P<0.05) than in those children without polymorphism. Among all the children with the polymorphism, the group born with LBW presented higher level of lipid peroxides (P<0.05).

The linear correlations between caspasa 3 and serum cholesterol (r=−0.999, P<0.05), lipid peroxides and susceptibility of infection (r=−0.769, P<0.05),

Conclusion: In children more susceptible for atheroscerosis in adulthood due to low birth weight the L162V mutation in PPAR are connected with a protective effect on lipid pattern

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