Abstract
The role of growth hormone (GH) in human fertility is widely debated with some studies demonstrating improvements in oocyte yield, enhanced embryo quality, and in some cases increased live births with concomitant decreases in miscarriage rates. However, the basic biological mechanisms leading to these clinical differences are not well-understood. GH and the closely-related insulin-like growth factor (IGF) promote body growth and development via action on key metabolic organs including the liver, skeletal muscle, and bone. In addition, their expression and that of their complementary receptors have also been detected in various reproductive tissues including the oocyte, granulosa, and testicular cells. Therefore, the GH/IGF axis may directly regulate female and male gamete development, their quality, and ultimately competence for implantation. The ability of GH and IGF to modulate key signal transduction pathways such as the MAP kinase/ERK, Jak/STAT, and the PI3K/Akt pathway along with the subsequent effects on cell division and steroidogenesis indicates that these growth factors are centrally located to alter cell fate during proliferation and survival. In this review, we will explore the function of GH and IGF in regulating normal ovarian and testicular physiology, while also investigating the effects on cell signal transduction pathways with subsequent changes in cell proliferation and steroidogenesis. The aim is to clarify the role of GH in human fertility from a molecular and biochemical point of view.
Highlights
Growth hormone (GH) is a 191 amino acid protein, which binds readily to the growth hormone receptor (GHR) and in some species the prolactin receptor [1, 2]
The GHR is a member of the cytokine receptor superfamily [3] and the majority of human GHR has been detected in the liver, it has been found to be abundantly expressed in all cellular components of the human ovary and testes [4, 5]
GH was demonstrated to have both direct and indirect effects on ovarian and testicular function, with direct effects mediated by the explicit GH-GHR interactions, while indirect effects likely to be mediated through the local production of secondary factors, Insulin-like growth factor (IGF) [6], a protein that is typically produced by the liver in response to GH stimulation [1, 7, 8]
Summary
Growth hormone (GH) is a 191 amino acid protein, which binds readily to the growth hormone receptor (GHR) and in some species the prolactin receptor [1, 2]. CREB binds cAMP response elements (CRE) in genomic DNA causing the transcription of various genes including those encoding for steroidogenic enzymes (e.g., aromatase) and cholesterol transport, the FIGURE 2 | A summary of the major GH and IGF signaling networks in female (theca/granulosa cell) and male (Leydig/Sertoli cell) reproductive physiology Both GH and IGF can activate PLC/PKC and PI3K/Akt pathways that cross-talk with FSHR and LHR signaling via cAMP/PKA to promote steroidogenesis and cell proliferation. The reported effect of GH on FSHR and LHR expression in vitro [31] and in vivo [38] is not trivial This indicated that GH may modify or potentiate the sensitivity of granulosa cells and/or theca cells to gonadotropin stimulation and subsequently regulate sex steroid synthesis and release in follicles, which boosts cell growth as paracrine/autocrine steroidogenic factors (Figure 1) [39].
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