Mitochondrial DNA depletion in small- and large-for-gestational-age newborns.

C GEMMA; SOOKOIAN, S.; J. ALVARIÑAS; L QUINTANA; GARCIA, SILVIA I; D,, K.; GONZALEZ, CLAUDIO; CARLOS JOSE PIROLA

Obesity

NAASO, The obesity Society,

Lugar: Silver Spring, MD, USA; Año: 2006 vol. 14 p. 2193 - 2199

1930-7381

Objective: to investigate whether mitochondrial DNA (mtDNA) content may be associated with clinical features, anthropometric variables and laboratory findings in both extremes of abnormal fetal growth: small and large for gestational age. Subjects: Eighty-eight pregnant women and their babies were included in a cross sectional study. According to the offspring birth weight normalized by sex and gestational age, there were 57 newborns with appropriate weight for gestational age (AGA) and 31 with abnormal weight for gestational age: 17 small for gestational age (SGA) and 14 large for gestational age (LGA). Methods: mtDNA quantification using nuclear DNA as a reference was measured by a real-time quantitative PCR method. Results: maternal pre-gestational BMI was associated with the weight of their offspring showing that SGA babies had lean mothers (BMI: 21.4±0.7) and LGA babies had overweight mothers (BMI 26.7±1.4) in comparison with AGA babies (BMI: 23.0±0.7), p <0.003. Newborn leptin levels were associated with birth weight adjusted by sex and gestational age, (SGA: 7.0±1.1 ng/mL, AGA: 15.2±1.6 ng/mL and LGA: 25.6±4.1 ng/mL, p<0.002). Conversely, mtDNA/nDNA ratio was significantly lower in both extremes of abnormal fetal growth: SGA (18±6) and LGA at birth (9±2) in comparison with AGA weight infants (28±4), (p< 0.03). Discussion: Our findings showed that mtDNA content decreased in newborns with abnormal weight in comparison with AGA babies. Based on a cumulative body of evidence, we might speculate that mtDNA depletion may be one of the putative links between abnormal fetal growth and metabolic and cardiovascular complications in later life.