Origin, proliferation and differentiation of Leydig cells

Lejeune, Hervé; Habert, René; Saez, J.M.

doi:10.1677/jme.0.0200001

Cited by 110 publications

(72 citation statements)

References 233 publications

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“…This increase reaches a peak in the third month. Afterwards, reduction and apopytosis occur in fetal and infantile Leydig cells (9)(10)(11). Inhibin-B is a glycoprotein belonging to the family of transforming growth factor beta (TGF-β) and is released from Sertoli cells in the prepubertal period.…”

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confidence: 99%

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Mini puberty and its interpretation

Kurtoğlu

Baştuğ

2014

Turk Arch Ped

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Gonadotropins which are at high levels in the middle of the fetal life are considerably low in the cord blood and estrogen is measured to be high. The reason for this is the inhibitory effect of increased estrogen levels in the circulation arising from the placenta on gonadotropin releasing hormone (GnRH) pulse generator and pituitary gonadotropins (1, 2). In male fetuses, testosterone levels probably contribute additionally to inhibition (3). Gonadotropin inhibition discontinues with placental seperation, the hypothalamo-pituitary-gonadal axis is activated and the hormonal changes which occur are identified as mini puberty (2, 4). The activation of the hypothalamo-pituitary-gonadal axis reach a peak level approximately in the 6-8th week after delivery. In this period, the levels of sex steroids are similar to early-middle pubertal levels, but their peripheral effects are not realized (4).In boys, the level of luteinizing hormone (LH) increases approximately 10-fold in the minutes following delivery and the level of tesosterone increases. This state lasts approximately for 12 hours (5, 6). The increase in follicle stimulating hormone (FSH) and LH continues in the second week after delivery, reaches a peak in the 4-10 th week, decreases in the 6 th month to the prepubertal levels. The level of testosterone increased by release of luteinizing hormone reaches a peak at around the third month and decreases to the prepubertal levels in the 6-9 th months (1,7,8). Similarly, the levels of 17-hydroxyprogesteron and androstenodione which are increased with testosterone decrease with reduction of the level of LH (2). After delivery, an increase in the number of Leydig cells starts. This increase reaches a peak in the third month. Afterwards, reduction and apopytosis occur in fetal and infantile Leydig cells (9-11). Inhibin-B is a glycoprotein belonging to the family of transforming growth factor beta (TGF-β) and is released from Sertoli cells in the prepubertal period. It is considered an indicator of sertoli cell function in prepubertal male children, but it does not reflect the number and function of germ cells. Inhibin-B acts as a regulator of release of FSH (1). Inhibin-B can be measured in the cord blood, it increases after delivery, reaches a peak in the 4-12 th month (exceeds the male adult level). It is at a considerably low level at the age of 3-9 years and increases again with the initiation of the puberty (3, 7). Serum inhibin-B levels are low in cases of hypogonadotropic hypogonadism (1, 12).Anti-Mullerian hormone (AMH) is a glycoprotein released from the sertoli cells starting from the fetal period. It is found in the cord blood and its level increases in the first 30 months after delivery. It reaches a peak in the 6 th month, starts to decrease Mini puberty and its interpretation AbstractGonadotropins which are high in the middle of the fetal life are measured to be considerably low in the cord blood and estrogen is found to be high in the cord blood. Gonodotropins are supressed by estrogen. After delivery,...

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confidence: 99%

“…Inhibin-B acts as a regulator of release of FSH (1). Inhibin-B can be measured in the cord blood, it increases after delivery, reaches a peak in the [4][5][6][7][8][9][10][11][12] th month (exceeds the male adult level). It is at a considerably low level at the age of 3-9 years and increases again with the initiation of the puberty (3,7).…”

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confidence: 99%

Mini puberty and its interpretation

Kurtoğlu

Baştuğ

2014

Turk Arch Ped

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“…On day 21 of postnatal life, the testicular interstitial tissue is populated by fetal Leydig cells, which appear around 14 dpc and differ morphologically and functionally at 15.5 dpc (Lejeune et al, 1998;Ariyaratne et al, 2000;Mendis-Handagama and Ariyaratne, 2001;Chen et al, 2009). Thus, for the prenatal undernourished group and the undernourished group, this differentiation occurred in a low availability of protein environment and resulted in low testosterone production.…”

Section: Discussionmentioning

confidence: 99%

“…Thereby, the number of Sertoli cells in maturation will determine the future sperm production (Hess and França, 2008). Similarly, testosterone production necessary for spermatogenic initiation and maintenance of reproductive functions will depend both on the individual steroidogenic capacity of each Leydig cell as on cell number per testis (Benton et al, 1995;Ge and Hardy, 1997;Lejeune, 1998;Chen et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Histomorphometric evaluation of the testicular parenchyma of rats submittedto protein restriction during intrauterine and postnatal life

Oliveira¹,

Silva²,

Souza³

et al. 2017

Turk J Biol

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The critical period of development is highly susceptible to disorders. Environmental contaminants, stress, and poor nutrition may permanently affect structurally and functionally an organism during adulthood. Protein restriction in intrauterine and neonatal periods may impair testicular cells and reduce steroidogenic activity. The current study investigated the effect of low protein diet during intrauterine and postnatal life on testicular function in immature and adult rats. Pregnant Wistar rats were fed either a normal protein diet or a low protein diet during pregnancy until birth and during lactation until weaning. The results showed that undernutrition during intrauterine life reduced epithelium height, tubular volume, Leydig cell volume, and serum testosterone levels, although it increased the support capacity of Sertoli cells. Tubular diameter, tubular volume, epithelium height, and Leydig cell population decreased when protein was restricted during lactation. Pregnant rats submitted to a low protein diet during the two periods generated male rats with a reduction in seminiferous tubule volume and length, Sertoli cell population, Leydig cell population and volume, and sperm production. Undernutrition during both the intrauterine and postnatal periods caused the most drastic testicular effects, as irreversible damage to Sertoli cell population and, consequently, to sperm production in the adult male.

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“…The hypothalamic-pituitary-gonadal axis stimulates testis development and testicular steroidogenesis in a cascade of precisely timed events (Lejeune et al, 1998). In the prepubertal boar, the testis remains morphologically silent until the animal is~12 weeks old.…”

Section: Introductionmentioning

confidence: 99%

Gene expression during testis development in Duroc boars

Lervik

Kristoffersen

Conley

et al. 2015

Animal

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Androstenone is a steroid pheromone occurring in the pubertal Leydig cells. Breeding against androstenone can decrease pheromone odour in swine meat but appears to cause unwanted side effects such as delayed onset of puberty. To study causality, global gene expression in developing boar testes at 12, 16, 20 and 27 weeks was investigated using a porcine cDNA microarray. The morphological status and androgenic levels of the same individuals have been described in a previous publication. In the present paper, expression of genes and pathways has been analysed with reference to these findings. Nine clusters of genes with significant differential expression over time and 49 functional charts were found in the analysed testis samples. Prominent pathways in the prepubertal testis were associated with tissue renewal, cell respiration and increased endocytocis. E-cadherines may be associated with the onset of pubertal development. With elevated steroidogenesis (weeks 16 to 27), there was an increase in the expression of genes in the MAPK pathway, STAR and its analogue STARD6. A pubertal shift in genes coding for cellular cholesterol transport was observed. Increased expression of meiotic pathways coincided with the morphological onset of puberty. Puberty-related change in Ca (2+) pathway transcripts, neurosteroids, neuronal changes and signalling in redox pathways suggested a developmental-specific period of neuromorphogenesis. Several growth factors were found to increase differentially over time as the testis matured. There may be interactions between MAPK, STAR and growth factors during specific periods. In conclusion, pathways for neurogenesis, morphological pathways and several transcripts for growth factors, which have known modulating effects on steroidogenesis and gonadotropins in humans and rodents, act at specific ages and developmental stages in the boar testis. The age dependency and complexity shown for development-specific testis transcripts must be considered when selecting phenotypic parameters for genetic selection for low androstenone. The results of selection based on measurement of phenotypic maturation and androstenone (or other steroid) levels at one specific age may differ depending on the age used. More research is necessary to find the optimal phenotype to use in order to reduce the unwanted side effects.

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Origin, proliferation and differentiation of Leydig cells

Cited by 110 publications

References 233 publications

Mini puberty and its interpretation

Mini puberty and its interpretation

Histomorphometric evaluation of the testicular parenchyma of rats submittedto protein restriction during intrauterine and postnatal life

Gene expression during testis development in Duroc boars

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