Hormonal findings in obese children. A review

Serum thyroid hormones in childhood obesity are not altered but caloric intake affects monoiodination of T4 to T3 and rT3. Plasma cortisol and urinary free cortisol concentrations are normal. Increase in cortisol production and secretion rate is reflected in increased values of urinary 17-hydroxycorticosteroids. Elevated urinary 17-ketosteroids are caused by increased androgen synthesis accounting for the increased height velocity in obese preadolescents and for the accelerated skeletal maturation. In both sexes earlier onset of puberty is noticed without remarkable alterations in gonadal steroids. Whether altered prolactin concentrations reflect neuroendocrine abnormalities remains unclear. Impairment of growth hormone release in face of normal or high somatomedins is not of clinical significance. Basal and stimulated insulin concentrations are high. Insulin resistance exists because glucose tolerance is simultaneously impaired. This is due to reduction in insulin receptor numbers and post-receptor defects in insulin action. Weight loss is effective in normalizing the above mentioned hormonal defects.