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The Consequences of Altered Somatotropic System on Reproduction

Abstract
Although the primary control of gonadotropin secretion is by the hypothalamic GnRH and the gonadal function is controlled by the pituitary gonadotropins and prolactin, the emerging evidence suggest a vital role of the somatotropic axis, growth hormone (GH) and insulin-like growth factor-I (IGF-I) in the control of the pituitary and gonadal functions. It has been shown that GH deficiency, GH resistance, and experimental alterations in IGF-I secretion modify folliculogenesis, ovarian maturation, ovulation and pregnancy, and in the male, GH/IGF-I plays an important role in spermatogenesis and the Leydig cell function. The primary focus of this review is to examine the role of GH/IGF-I on the onset of puberty, fertility, pituitary, and gonadal endocrine functions. A number of studies have revealed that fertility is affected in GH-deficient dwarf and in IGF-I gene ablated mice, possibly due to subnormal function of either the pituitary gland or the gonads. In the female GH receptor gene knockout (GHR-KO) mice, there was impairment in follicular development, ovulation rate, sexual maturation, production of and responsiveness to pheromonal signals, and the corpus luteum function. In IGF-I- deficient male GHR-KO mice, the puberty is delayed, the spermatogenesis is affected, and the neuroendocrine-gonadal function is attenuated. Similarly, in some of the human Laron syndrome patients the puberty is delayed due to GH resistance. These data suggest that in addition to GnRH and gonadotropins, GH/IGF-I influence the pituitary and gonadal functions in animals and humans.

Key words: Neuroendocrinology • Ovary • Testis • Growth hormone • Pituitary hormones

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