The regulation of growth and reproduction has been investigated using murine and non-human primate models. It has been established that locally produced insulin-like growth factor 1 (IGF1) regulates postnatal brain growth by augmenting neuronal metabolism . Signal pathways similar to those used by insulin in the periphery are activated by IGF1 in the brain to stimulate glucose uptake, phosphorylation and incorporation into glycogen. It has also been demonstrated that contrary to the common assumption, IGF1 does not play a major role in brain myelination. These findings help to explain the etiology of mental retardation in individuals with genetic defects in IGF1 synthesis. Study of the epiphysial growth plate in IGF1- and IGF2-deficient mice has shown that these two peptides act in distinct and complementary ways to enhance long bone growth. IGF2 stimulates chondrocyte proliferation and IGF1 stimulates chondrocyte hypertrophy. Thus, the two related growth factors synergistically augment the growth plate expansion which underlies long bone growth and achievement of maximal adult stature. In the study of reproduction, it has been shown that androgens stimulate early stages of ovarian follicle development. Activation of ovarian androgen receptors stimulates IGF1 and IGF1 receptor expression which, in turn, stimulates follicle growth. This is the first information uncovering the mechanisms involved in the initiation of ovarian follicle growth. It has also been demonstrated that local IGF1 expression is necessary for completion of estrogen- induced uterine cell cycle, with arrest of mitosis in G2 in the absence of IGF1. This is the first evidence implicating extracellular signaling by growth factors in the regulation of late phases of the cell cycle. - growth, reproduction, insulin-like growth factor I (IGF1), brain growth, growth plate, androgens, ovarian follicle development, cell cycle
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