ABSTRACT
OBJECTIVE: To correlate, in a sample of healthy children and adolescents, the activity of the enzyme acid phosphatase (ACP) with its different genetic phenotypes and of these with some cardiovascular risk parameters such as body mass index (BMI), percentage of total fat mass (%TFM), trunk fat (TF), insulin resistance, and the arterial blood pressure (BP). DESIGN AND METHODS: The sample was composed of 173 healthy children and adolescents, 96 (55.5%) F and 77 (44.5%) M, with ages between 10 and 16 years (mean: 13.04 +/- 1.68). The ACP activity was determined through a spectrophotometric method and its phenotypes through isoelectric focusing electrophoresis. BMI (Kg/m2) and the BP were obtained by standardized methods. Glycemia determined by the glucose oxidase method and insulinemia by RIA method. Insulin resistance based on the homeostasis model assessment (HOMA) was calculated as: [fasting insulin (microU/ml) x fasting glucose (mmol/l)]: 22.5. The %TFM and TF were determined by dual energy x-ray absorptiometry (DXA). The statistical methods used were ANOVA, the Pearson correlation and the Student's test. RESULTS: The distribution of the phenotypes were the following--absolute versus relative frequencies: BB-74 (48.4%), AB-52 (34%), AA-16 (10.5%), BC-7 (4.6%), AC-3 (2%) and CC-1 (0.7%). ACP activities (mean: 321.04 +/- 84.56) were significantly different among the phenotypes (p < 0.001). The smallest activity was observed in the AA individuals, the highest in CC, followed by BC (247.17 +/- 66.52 and 767.30 and 362.44 +/- 91.56 respectively). Glycemia was higher in the AA individuals (4.61 +/- 0.37) compared to CC + BC (4.40 +/- 0.31) (p = 0.08). A direct correlation was verified between HOMA and BP, both diastolic (p = 0.013, r = 0.250) and systolic (p = 0.015, r = 0.246), as well as of these with BMI (mean: 20.57 +/- 3.24) and insulinemia (p = 0.016, r = 0.215; p = 0.004, r = 0.280 and p = 0.007, r = 0.240; p = 0.008, r = 0.261 respectively for diastolic and systolic BP). There were no significant difference of BMI between sexes, nor of this as well as of % TFM and TF among the different genetic phenotypes of ACP. CONCLUSIONS: The smallest enzymatic activity of ACP seems to be associated with the AA individuals, where a trend for higher glycemia was verified. BMI, HOMA and insulinemia, due to their significant direct relationship with diastolic and systolic BP in this sample of children and adolescents may warrant more future attention in the evaluation of cardiovascular risk. There were no significant differences of HOMA, BMI, %TFM, TF nor of BP among the different ACP genetic phenotypes.
