Obesity during childhood can significantly impact growth and puberty Summary Obese children show accelerated linear growth during pre-puberty possibly due to early estrogenization, normal /high IGF1 levels, high leptin levels and the action of insulin on the IGF1 receptor. Obesity also affects puberty leading to both earlier onset of puberty in girls and alteration in pubertal timing in boys combined with reduced growth spurt. Leptin has been identified as the most significant link between obesity and pubertal onset. During puberty increased estrogen levels antagonize the growth-promoting actions of leptin and accelerate bone maturation, leading to earlier epiphyseal closure. Spontaneous and stimulated GH secretion, is markedly reduced in obesity due to hypothalamic, pituitary and peripheral factors. The blunted GH response to stimuli may lead to overdiagnosis of growth hormone deficiency (GHD) in obese short-statured children. While obese children may be taller during childhood, they have reduced growth spurt during puberty due to accelerated epiphyseal closure and final heights are similar or even compromised compared to the genetic potential. GH secretion both spontaneous and stimulated is decreased, and therefore the differential diagnosis of GHD versus an obesity-related decrease in GH secretion remains a problem of great practical importance. Data on the effects of obesity on GH levels are limited and weight-status adjusted cutoffs for GH stimulation tests have not been set and validated as yet. This review summarizes our knowledge on the underlying mechanisms by which obesity affects growth and puberty and data on its impact on GH stimulation tests.
Karachaliou et al. (Fri,) studied this question.