Stimulation of Steroidogenesis in Immature Rat Leydig Cells Evoked by Interleukin-1α Is Potentiated by Growth Hormone and Insulin-Like Growth Factors

Colón, Eugenia; Svechnikov, Konstantin; Carlsson-Skwirut, Christine; Bang, Peter; Söder, Olle

doi:10.1210/en.2004-0485

Cited by 40 publications

(40 citation statements)

References 64 publications

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“…Shortly after the testicular phenotype of the NKX2-1 null mice was described, we reported that fetal mouse Leydig cells express the melanocortin type 2 receptor, the receptor for ACTH. Furthermore, we showed that ACTH would stimulate androgen production in fetal and neonatal testes but not in adult (Amir et al 1978, Weiss-Messer et al 1996, Colon et al 2005), but there is little evidence of effects on the fetal Leydig cells. In the human fetus, the second trimester pituitary secretes prolactin (PRL), and the PRL receptor is expressed in the testis, but there is no correlation between PRL and testosterone (Fowler et al 2008(Fowler et al , 2009).…”

Section: Endocrinology Of the Fetal Testismentioning

confidence: 76%

Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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The testes are essential endocrine regulators of fetal masculinization and male development and are, themselves, subject to hormonal regulation during gestation. This review focuses, primarily, on this latter control of testicular function. Data available suggest that, in most mammalian species, the testis goes through a period of independent function before the fetal hypothalamic-pituitary-gonadal axis develops at around 50% of gestation. This pituitary-independent phase coincides with the most critical period of fetal masculinization. Thereafter, the fetal testes appear to become pituitary hormone-dependent, concurrent with declining Leydig cell function, but increasing Sertoli cell numbers. The two orders of mammals most commonly used for these types of studies (rodents and primates) appear to represent special cases within this general hypothesis. In terms of testicular function, rodents are born 'early' before the pituitary-dependent phase of fetal development, while the primate testis is dependent upon placental gonadotropin released during the pituitary-independent phase of development.

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Section: Endocrinology Of the Fetal Testismentioning

confidence: 76%

Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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“…In line with this hypothesis, boys with a genetic deficiency in production of this growth factor are undermasculinized, suggesting a lack of androgen production by their fetal Leydig cells [30]. As stated above GH and IGF-I may also act as survival factors for Leydig cells [31,32]. Thus, all of these factors appear to work in concert to trigger the processes that control the differentiation, maturation and regression of human fetal Leydig cells.…”

Section: Developmental Regulation Of Fetal Human Leydig Cellsmentioning

confidence: 94%

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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“…Even though most of the physiologic functions of IGF-I are thought to occur via IGFR (29), surprisingly, in newborn testes only moderate staining of IGFR in ICs and LCs was observed, whereas during the postnatal activation period, poor expression was also found in LCs. It is interesting that, Colon et al (16) recently found that both IGF-II and insulin phosphorylate/activate rat testis IGFR in the same manner as IGF-I, suggesting that all of these factors activate common signaling pathways in LCs.…”

Section: Discussionmentioning

confidence: 99%

“…Growth factors such as IGF and insulin through endocrine, autocrine, and paracrine regulatory events are known to play diverse roles in steroidogenesis (16,23,35). Hence, it could be proposed that, in the absence of LH, IGFs, via IGFR and/or IR, might induce the synthesis of androgens in precursor LC fibroblast.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, even though GH receptor (GHR) mRNA expression has been detected in human testicular tissue (15), its immunolocalization in human prepubertal testis has not been determined. In addition, it has been recently demonstrated that IGF-II is able to regulate steroidogenesis in rat LCs (16). Therefore, a role for either IGF-I or IGF-II on precursor or immature LC differentiation, via IGF receptor (IGFR), could be proposed.…”

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confidence: 99%

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

et al. 2008

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Immunoexpression of IGF-I, IGF-II, type 1 IGF receptor (IGFR), insulin receptor (IR), and GH receptor (GHR) was analyzed in human testis, in three age groups (Gr): Gr1 (neonates), Gr2 (postnatal testicular activation), and Gr3 (early prepuberty). In interstitial cells, low IGF-I and GHR, but moderate IR immunoexpression was observed in all Grs. However, high expression of IGF-II in Gr1, and moderate expression of IGFR in Gr1 and Gr2 were found. In Leydig cell (LC), high expression of IGF-II, moderate expression of IGFR and GHR, and undetectable IGF-I was found. Moreover, IR was highly expressed in Gr2. The effect of IGF-I on cell proliferation (PI) and apoptosis (AI), induction of cytochrome P450 side chain cleavage (cP450scc) immunoexpression, 3␤-hydroxysteroid dehydrogenase mRNA and testosterone (T) secretion was evaluated in human testis cell cultures. IGF-I increased P450scc immunoexpression, 3␤-hydroxysteroid dehydrogenase mRNA, T secretion, and PI, but decreased AI. We propose that IGF-II, mainly through IR, is involved in functional LC differentiation. In some interstitial cells, probably in LC precursors, IGF-II/IR could be involved, among other factors, in the stimulation of PI and/or inhibition of AI, and in LC differentiation. (Pediatr Res 63: 662-666, 2008)

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Stimulation of Steroidogenesis in Immature Rat Leydig Cells Evoked by Interleukin-1α Is Potentiated by Growth Hormone and Insulin-Like Growth Factors

Cited by 40 publications

References 64 publications

Endocrinology of the mammalian fetal testis

Endocrinology of the mammalian fetal testis

Origin, Development and Regulation of Human Leydig Cells

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

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