NEONATAL SOCIETY ABSTRACTS
A study of the relationship between serum angiotensin-converting enzyme (ACE) concentration, ACE genotype, and markers of insulin resistance in premature infants
Presented at the Neonatal Society 2006 Summer Meeting (programme).
Mills L1, Redpath S1, Wallace M2, Jackson L1
1 Neonatal Unit, Princess Royal Maternity Hospital, Glasgow, UK
2 Department of Biochemistry, Glasgow Royal Infirmary, Glasgow, UK
Background: Angiotensin Converting Enzyme (ACE) genotype and Renin-Angiotensin (RAAS) axis activity may influence insulin-resistance and birth weight in humans. Polymorphisms of the ACE gene are common and the insertion-insertion (II) genotype has been associated with low birth weight and relative insulin-resistance in adulthood, yet no data exists for children.
Objectives: To evaluate the possible relationship between ACE insertion-deletion (ID) genotype, ACE level, and insulin resistance in a cohort of premature infants at 1 yr corrected gestational age.
Methods: Fasting insulin and glucose concentrations were obtained from a cohort of premature infants at the time of discharge from the neonatal unit and repeated at one year of age. Additional blood samples were obtained at one year of age for ACE level and genotype as well as HDL cholesterol and fasting triglycerides. A logarithmic transformation of the fasting glucose and insulin concentration was calculated, the QUICKI, as an estimate of relative insulin resistance. Simple correlation was used to identify relationships between ACE genotype and biochemical markers. Differences between groups were determined by parametric (independent t test) or non-parametric techniques (Mann-Whitney U test) depending on their distribution. Analysis was performed using SPSS.
Results: Forty infants participated (23 male; 17 female). Mean Birthweight 1.49kg (range 0.54kg-2.56kg). At one year of age, ACE genotype correlated with fasting insulin (r=-0.46, p=0.01), QUICKI (r=0.38, p=0.03) and ACE level (r=0.54, p<0.01). 7 infants had ACE genotype II, 25 infants ID and 7 infants DD. Infants with the ACE genotype II had surrogate markers of insulin-resistance relative to those with other genotypes (ID, DD): fasting insulin concentration (mean 14.7 vs 7.4 mU/L, U=36.5, p<0.01) and QUICKI (mean 0.55 vs 0.70, U=44.5, p=0.03). Infants with II genotype also had significantly lower ACE levels than those with ID and DD (mean 34.86 vs. 65.69, t(36)=-7.57, p<0.01).
Conclusions: At one year of age polymorphisms of the ACE genotype appear to influence markers of insulin resistance and ACE activity in keeping with that described in adult populations.