ACTA ENDOCRINOLOGICA (BUC)

Introduction: Obesity, a disease whose morphological background has as main problem the “dysfunctional” adipocyte, continues to raise scientific interest for the completion of the existing data and the verification of the hypothetic ones. Material and method: We determined insulinemia and glycemia within the oral glucose tolerance test (OGTT), and we analyzed the relation between the fat mass and cortisolemia in a group of 50 obese patients aged between 4 months –18 years. In 19 obese patients, between 5 ½ -17 ½ years old, we determined the basal leptin and resistin serum levels, comparatively to a control group of 19 normal weight children. In 14 obese and 10 normal weight controls, we determined the number of androgenic and estrogenic adipocyte receptors, which we correlated with the degree of obesity, the Tanner stage and respectively the testosterone, progesterone and estradiol serum levels. We studied the cellularity, morphohistochemical and ultrastructural features of the adipose tissue in 42 obese and 20 normal weight controls. Leptin and resistin were determined by ELISA. The measurement of the fat mass was done by bioelectric impedance. For the study of the adipose tissue we took 1g of tissue from the retro-trochanterian area. We identified the estrogenic (ER) and androgenic (AR) receptors by LSAB2 technique. We interpreted the data statistically by the linear regression analysis and variance test “t” for two unequal parameters using Microsoft Excel 2002. Results: A positive correlation was demonstrated between glycemias and insulinemias for the entire group (r=0.927, p=0.002), as well as between cortisolemia and fat mass excess (r=0.917; p=0.001). Serum leptin levels were significantly high in the obese (mean values: 81.07 ng/ml) comparatively to normal weight individuals (mean values: 4.17 ng/ml). Resistin serum levels did not show significant differences between the obese and normal weight individuals. We cannot talk about the existence of any correlation between resistin and leptin.