Role of IGFs and Insulin in the Human Testis During Postnatal Activation: Differentiation of Steroidogenic Cells

Berensztein, Esperanza; Baquedano, María Sonia; Pepe, Carolina; Costanzo, Mariana; Saraco, Nora; Ponzio, Roberto; Rivarola, Marco A.; Belgorosky, Alicia

doi:10.1203/pdr.0b013e31816c8ffc

Cited by 33 publications

(23 citation statements)

References 37 publications

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“…In fact, in experimental conditions GH regulates Sertoli cell function [39] and IGF-I and IGF-II regulate testicular interstitial cell steroidogenesis, proliferation and apoptosis [40]. …”

Section: Amh Levels In Prepubertal Male Hypogonadismmentioning

confidence: 99%

Anti-Müllerian Hormone and Sertoli Cell Function in Paediatric Male Hypogonadism

2010

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In the prepubertal male, Sertoli cells are the most active testicular cell population. Without stimulation tests, prepubertal hypogonadism can only be evidenced if Sertoli cell function is assessed. Anti-müllerian hormone (AMH) is a distinctive marker of the prepubertal Sertoli cell. Serum AMH is high from fetal life until puberty. In postnatal life, AMH testicular production is stimulated by FSH and potently inhibited by androgens. In anorchid patients, AMH is undetectable. In prepubertal males with fetal- or childhood-onset primary or central hypogonadism affecting the whole gonad, serum AMH is low. Conversely, when hypogonadism only affects Leydig cells (i.e., LH/human chorionic gonadotrophin receptor or steroidogenic enzyme defects), serum AMH is normal/high. AMH is also normal/high in patients with androgen insensitivity. In patients of pubertal age with central hypogonadism, AMH is low for Tanner stage – reflecting lack of FSH stimulus, – but high for age – reflecting lack of testosterone inhibitory effect. FSH treatment results in serum AMH rise, whereas human chorionic gonadotrophin treatment increases testosterone levels which inhibit AMH production. In conclusion, AMH determination is helpful in assessing gonadal function, without need for stimulation tests, and orientates the aetiological diagnosis of paediatric male hypogonadism. Furthermore, serum AMH is an excellent marker of FSH and androgen action in the testis.

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“…In fact, in experimental conditions GH regulates Sertoli cell function [39] and IGF-I and IGF-II regulate testicular interstitial cell steroidogenesis, proliferation and apoptosis [40]. …”

Section: Amh Levels In Prepubertal Male Hypogonadismmentioning

confidence: 99%

Anti-Müllerian Hormone and Sertoli Cell Function in Paediatric Male Hypogonadism

2010

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“…Furthermore, some evidence suggests that ligands of the IGF system affect the differentiation and steroidogenic capacity of fetal Leydig cells, both in rodents and humans [28,29]. In the human testis, IGFs and the type I IGF receptor are differentially expressed at different maturational stages and seem to be involved in the regulation of Leydig cell proliferation and survival, and steroidogenic maturation [29].…”

Section: Developmental Regulation Of Fetal Human Leydig Cellsmentioning

confidence: 99%

Origin, Development and Regulation of Human Leydig Cells

et al. 2010

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Sex steroids are crucial regulators of sexual differentiation and the proper development of secondary sex characteristics and patterns of sexual behavior. Since Leydig cells are the primary major producers of these steroid hormones, maintenance of the normal functions of these cells determines the reproductive capacity and fertility of males. The present minireview discusses recent findings concerning endocrine and paracrine regulation of the proliferation, differentiation and involution of human Leydig cells. The physiology and function of the two distinct fetal and adult populations of human Leydig cells are described, with particular focus on the paracrine environment that triggers their differentiation and functional maturation. The roles of established and more recently discovered paracrine regulators of this maturation, including insulin-like factor 3, platelet-derived growth factor-α, desert hedgehog, ghrelin and leptin are considered. A brief description of the origin, ontogenesis and functional markers of human fetal and adult Leydig cells is presented.

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“…[175][176][177] IGF-1 stimulates 5α-reductase, adrenal and gonadal androgen synthesis, AR signal transduction, sebocyte proliferation and lipogenesis. [178][179][180][181][182][183][184] Milk consumption results in a significant increase in IGF-1 serum level and exerts strong insulinotropic effects comparable to high glycaemic food. 185,186 Insulin induces hepatic IGF-1 secretion, and both hormones amplify the stimulatory effect of GH on sebocytes and augment mitogenic downstream signaling pathways of insulin receptors, IGF-1 receptor and FGFR2b (Fig.…”

Section: Interleukin-1α Network In Keratinocytesmentioning

confidence: 99%

Role of FGFR2-signaling in the pathogenesis of acne

Melnik

2009

Dermato-Endocrinology

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It is the purpose of this review to extend our understanding of the fibroblast growth factor (FGF) receptor-2b-signaling network in the pathogenesis of acne. A new concept of the role of FGFR2b-signaling in dermal-epithelial interaction for skin appendage formation, pilosebaceous follicle homeostasis, comedogenesis, sebaceous gland proliferation and lipogenesis is presented. The FGFR2-gain-of-function mutations in Apert syndrome and unilateral acneiform nevus are most helpful model diseases pointing the way to androgen-dependent dermalepithelial FGFR2-signaling in acne. Androgen-mediated upregulation of FGFR2b-signaling in acne-prone skin appears to be involved in the pathogenesis of acne vulgaris. In organotypic skin cultures, keratinocyte-derived interleukin-1α stimulated fibroblasts to secrete FGF7 which stimulated FGFR2b-mediated keratinocyte proliferation. Postnatal deletion of FGFR2b in mice resulted in severe sebaceous gland atrophy. The importance of FGFR2b in sebaceous gland physiology is further supported by the mode of action of anti-acne agents which have been proposed to attenuate FGFR2b-signaling. Downregulation of FGFR2b-signaling by isotretinoin explains its therapeutic effect in acne. Downregulation of FGFR2b-signaling during the first trimester of pregnancy disturbs branched morphogenesis and explains retinoid embryotoxicity. Insulin-like growth factor-1 (IGF-1), the mediator of growth hormone during puberty, intracts with androgen-dependent FGFR2b-signaling and links androgen-and FGF-mediated signal transduction important in sebaceous gland homeostasis. The search for a follicular defect in the dermalepithelial regulation of growth factor-signaling in acne-prone skin appears to be a most promising approach to clarify the pathogenesis of acne.

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Role of IGFs and Insulin in the Human Testis During Postnatal Activation: Differentiation of Steroidogenic Cells

Cited by 33 publications

References 37 publications

Anti-Müllerian Hormone and Sertoli Cell Function in Paediatric Male Hypogonadism

Anti-Müllerian Hormone and Sertoli Cell Function in Paediatric Male Hypogonadism

Origin, Development and Regulation of Human Leydig Cells

Role of FGFR2-signaling in the pathogenesis of acne

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