Endocrine - Gonad Development - Revision history

Z8600021 at 03:22, 20 Mayıs 2019

2019-05-20T03:22:19Z

← Older revision		Revision as of 13:22, 20 Mayıs 2019
Line 17:		Line 17:

	== Some Recent Findings ==		== Some Recent Findings ==
			[[File:Model male androsterone synthesis.jpg\|alt=Model male second trimester androsterone synthesis\|thumb\|Model male second trimester androsterone synthesis{{#pmid:30763313\|PMID30763313}}]]
	{\|		{\|
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"

Z8600021 at 01:48, 2 Mayıs 2019

2019-05-02T01:48:03Z

← Older revision		Revision as of 11:48, 2 Mayıs 2019
Line 2:		Line 2:
	==Introduction==		==Introduction==
	[[File:XXhpgaxis.jpg\|thumb\|Female HPG axis]]		[[File:XXhpgaxis.jpg\|thumb\|Female HPG axis]]
	The term gonad refers to both the female ~~[[Ovary Development\|~~ovary]] and the male ~~[[Testis Development\|~~testis]], ~~which~~ have their own topic pages.		The term gonad refers to both the female {{ovary}} and the male {{testis}}, both have their own detailed topic pages. This section of notes refers only to the development of the gonad as an endocrine organ.

	This section of notes refers only to the development of the gonad as an endocrine organ~~. A detailed description of the gonad development is covered in both [[Ovary Development]] and [[Testis Development]]~~.

	Embryonically, initial endocrine development of the testis is required for development of both the internal genital tract and the external genitalia.		Embryonically, initial endocrine development of the testis is required for development of both the internal genital tract and the external genitalia.

	Postnatally, the gonads are part of an integrated '''H'''ypothalamus-'''P'''ituitary-'''G'''onad (HPG) axis.		Postnatally, the gonads are part of an integrated '''H'''ypothalamus - '''P'''ituitary - '''G'''onad (HPG) axis. Post-puberty, this axis is the key regulator of the female reproductive cycle, the {{menstrual cycle}}.


	{{Endocrine Links}}		{{Endocrine Links}}
			<br>
			{{Menstrual_Links}}
			<br>
	{{Genital Links}}		{{Genital Links}}
			<br>

	== Some Recent Findings ==		== Some Recent Findings ==
Line 87:		Line 87:

	==Estrogen==		==Estrogen==
	{{~~Estrogen~~}}		{\|
			\| The estradiol ({{estrogen}}, oestrogen) hormone is a steroid sex hormone expressed in both male and female.

			estrogenic activity in human placental extracts was due to the presence of at least three compounds: estriol, estrone, and 17β-estradiol.

			In the female, this hormone together with progesterone regulate changes that occur each menstrual cycle. During female development the fetal adrenal gland cortex synthesises DHEA (and DHEA/S), an oestrogen precursor (see image [[:File:Fetal adrenal gland steroidogenesis.jpg\|Fetal adrenal gland steroidogenesis]]), converted by the {{placenta}} into estrogen compounds; estriol, estrone, and 17β-estradiol. During {{puberty}}, ovarian estrogen production is responsible for development of the secondary feminine sex characteristics.

			In the male, [[:File:Testis histology 2.jpg\|Leydig cells]] produce estrogen into the rete testis fluid at variable levels in different species. During male embryonic development exposure to high levels of estrogen can lead to genital abnormalities.

			\| [[File:Estradiol.jpg\|alt=estrogen\|300px]]

			Estradiol
			\|}

	==Progesterone==		==Progesterone==

	{{Progesterone}}		{\|
			\| The progesterone (progestin) hormone is produced by the granulosa cells of the ovarian follicles at different levels during the {{menstrual cycle}} and at high levels by the luteal cells (P4) of the {{corpus luteum}}.


			In 1934 progesterone (progestin) C<sub>21</sub>H<sub>30</sub>O<sub>2</sub> was first isolated from the {{corpus luteum}} and its structure reported by four separate groups of researchers.<ref name=Butenandt1934>Butenandt A. Neure Ergebnisse auf dem Gebiet der Sexualhormone. Wien Klin Wochenschr. 1934;47:936.</ref><ref name=Slotta1934>Slotta KH, Ruschig H, Fels E. Ȕber der Hormon aus dem Corpus-luteum. Ber Chem Ges. 1934;67:1270.</ref><ref name=Hartmann1934>Hartmann M, Wettstein A. Ein krystallisiertes Hormon aus Corpus-luteum. Helv Chim Acta. 1934;17:878.</ref>{{#pmid:17817057\|PMID17817057}}

			\| [[File:Progesterone.jpg\|alt=Progesterone molecular structure\|300px]]
			Progesterone molecular structure
			\|}

Z8600021 at 01:42, 2 Mayıs 2019

2019-05-02T01:42:35Z

← Older revision		Revision as of 11:42, 2 Mayıs 2019
Line 31:		Line 31:

	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Endocrine+Gonad+Development ''Endocrine Gonad Development''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Testosterone+Embryology ''Testosterone Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Granulosa+Cell+Embryology ''Granulosa Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Leydig+Cell+Embryology ''Leydig Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Interstitial+Cell+Embryology ''Interstitial Cell Embryology'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Endocrine+Gonad+Development ''Endocrine Gonad Development''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Testosterone+Embryology ''Testosterone Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Granulosa+Cell+Embryology ''Granulosa Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Leydig+Cell+Embryology ''Leydig Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Interstitial+Cell+Embryology ''Interstitial Cell Embryology'']


	\|}		\|}
Line 60:		Line 59:
	* X chromosome genes regulate ovary development		* X chromosome genes regulate ovary development

	==~~Male Hormone Levels~~==		==Steroidogenesis==

			[[File:Steroidogenesis.png\|600px\|Steroidogenesis]]

			==Testosterone==

	Testicular Leydig cells (interstitial cells) are the main source of testosterone in males.		Testicular Leydig cells (interstitial cells) are the main source of testosterone in males.

Line 72:		Line 76:
	Leydig cells stained for LHCGR1{{#pmid:18433292\|PMID18433292}}		Leydig cells stained for LHCGR1{{#pmid:18433292\|PMID18433292}}

	=~~=Steroidogenesis==~~		===Androgen and Digit ratio (2D:4D)===

	~~[[File:Steroidogenesis.png\|600px\|Steroidogenesis]]~~

	==Androgen and Digit ratio (2D:4D)==
	[[File:Finger_length_ratio_-_2D4D.jpg\|thumb\|Androgen and Digit ratio (2D:4D]]		[[File:Finger_length_ratio_-_2D4D.jpg\|thumb\|Androgen and Digit ratio (2D:4D]]
	The ratio of 2nd and 4th finger (D, digit) length. This ratio has been suggested to relate to high fetal [[T#testosterone\|testosterone]] concentration (males have lower 2D:4D than females) and has been shown for several species.{{#pmid:16504142\|PMID16504142}} Although a study in mice has not shown the same correlation.{{#pmid:19495421\|PMID19495421}} There have been some suggestions that the ratio may also be an indicator of various neurological abnormalities.		The ratio of 2nd and 4th finger (D, digit) length. This ratio has been suggested to relate to high fetal [[T#testosterone\|testosterone]] concentration (males have lower 2D:4D than females) and has been shown for several species.{{#pmid:16504142\|PMID16504142}} Although a study in mice has not shown the same correlation.{{#pmid:19495421\|PMID19495421}} There have been some suggestions that the ratio may also be an indicator of various neurological abnormalities.

	'''To measure (2D:4D)''' - using your right hand palm up, measure the index finger (2) and ring finger (4) length from palm to tip. Dividing the index finger by the ring finger gives the 2D:4D ratio, average women ratio is 1, average men is 0.98.		'''To measure (2D:4D)''' - using your right hand palm up, measure the index finger (2) and ring finger (4) length from palm to tip. Dividing the index finger by the ring finger gives the 2D:4D ratio, average women ratio is 1, average men is 0.98.

			==Anti-Mullerian Hormone==

			{{AMH}}

			==Estrogen==
			{{Estrogen}}

			==Progesterone==

			{{Progesterone}}


	:{{Genital Links}}		{{Genital Links}}

	==Adult Histology==		==Adult Histology==

Z8600021 at 01:47, 18 December 2018

2018-12-18T01:47:52Z

← Older revision		Revision as of 11:47, 18 December 2018
Line 30:		Line 30:
	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Endocrine+Gonad+Development ''Endocrine Gonad Development'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Endocrine+Gonad+Development ''Endocrine Gonad Development''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Testosterone+Embryology ''Testosterone Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Granulosa+Cell+Embryology ''Granulosa Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Leydig+Cell+Embryology ''Leydig Cell Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Interstitial+Cell+Embryology ''Interstitial Cell Embryology'']

	~~<pubmed limit=5>Endocrine Gonad Development</pubmed>~~

	\|}		\|}
Line 38:		Line 37:
	! Older papers		! Older papers
	\|-		\|-
	\|		\| {{Older papers}}
	* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''{{#pmid:22238103\|PMID22238103}} "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]		* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''{{#pmid:22238103\|PMID22238103}} "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
	\|}		\|}

Z8600021 at 02:55, 4 August 2018

2018-08-04T02:55:06Z

← Older revision		Revision as of 12:55, 4 August 2018
Line 20:		Line 20:
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
			* '''Transcriptional activity of oestrogen receptors in the course of embryo development'''{{#pmid:30012715\|PMID30012715}} "Oestrogens are well-known proliferation and differentiation factors that play an essential role in the correct development of sex-related organs and behaviour in mammals. With the use of the ERE-Luc reporter mouse model, we show herein that throughout mouse development, oestrogen receptors (ERs) are active starting from day 12 post conception. Most interestingly, we show that prenatal luciferase expression in each organ is proportionally different in relation to the germ layer of the origin. The luciferase content is highest in ectoderm-derived organs (such as brain and skin) and is lowest in endoderm-derived organs (such as liver, lung, thymus and intestine). Consistent with the testosterone surge occurring in male mice at the end of pregnancy, in the first 2 days after birth, we observed a significant increase in the luciferase content in several organs, including the liver, bone, gonads and hindbrain. The results of the present study show a widespread transcriptional activity of ERs in developing embryos, pointing to the potential contribution of these receptors in the development of non-reproductive as well as reproductive organs. Consequently, the findings reported here might be relevant in explaining the significant differences in male and female physiopathology reported by a growing number of studies and may underline the necessity for more systematic analyses aimed at the identification of the prenatal effects of drugs interfering with ER signalling, such as aromatase inhibitors or endocrine disrupter chemicals."

	* '''Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes'''{{#pmid:26929346\|PMID26929346}} "Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. ... The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor β (TGF-β). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-β, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage."		* '''Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes'''{{#pmid:26929346\|PMID26929346}} "Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. ... The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor β (TGF-β). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-β, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage."

	* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''{{#pmid:22238103\|PMID22238103}} "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
	\|}		\|}

Line 35:		Line 35:

	\|}		\|}
			{\| class="wikitable mw-collapsible mw-collapsed"
			! Older papers
			\|-
			\|
			* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''{{#pmid:22238103\|PMID22238103}} "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
			\|}

	HPG Axis - [http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A972&rendertype=box&id=A1057 Endocrinology - Simplified diagram of the actions of gonadotrophins]		HPG Axis - [http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A972&rendertype=box&id=A1057 Endocrinology - Simplified diagram of the actions of gonadotrophins]

Z8600021 at 13:11, 19 March 2018

2018-03-19T13:11:04Z

← Older revision		Revision as of 23:11, 19 March 2018
Line 20:		Line 20:
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes'''~~<ref name="~~PMID26929346~~"><pubmed>26929346</pubmed></ref>~~ "Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. ... The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor β (TGF-β). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-β, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage."		* '''Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes'''{{#pmid:26929346\|PMID26929346}} "Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. ... The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor β (TGF-β). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-β, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage."
	* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''~~<ref><pubmed>~~22238103~~</pubmed></ref>~~ "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
			* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''{{#pmid:22238103\|PMID22238103}} "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
	\|}		\|}

Line 58:		Line 59:
	[[File:Male_testosterone_and_AMH_level_graph.jpg\|600px]]		[[File:Male_testosterone_and_AMH_level_graph.jpg\|600px]]

	Human Male Testosterone and Anti-Müllerian Hormone (AMH) relative levels~~<ref><pubmed>~~16544032~~</pubmed>~~\| ~~[http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302005000100005&lng=en&nrm=iso&tlng=en Arq Bras Endocrinol Metabol.]</ref>~~		Human Male Testosterone and Anti-Müllerian Hormone (AMH) relative levels{{#pmid:16544032\|PMID16544032}}

	===Leydig Cells===		===Leydig Cells===
	[[File:Leydig cells stained for LHCGR1.jpg\|400px]]		[[File:Leydig cells stained for LHCGR1.jpg\|400px]]

	Leydig cells stained for LHCGR1~~<ref name="~~PMID18433292~~"><pubmed>18433292</pubmed></ref>~~		Leydig cells stained for LHCGR1{{#pmid:18433292\|PMID18433292}}

	==Steroidogenesis==		==Steroidogenesis==
Line 71:		Line 72:
	==Androgen and Digit ratio (2D:4D)==		==Androgen and Digit ratio (2D:4D)==
	[[File:Finger_length_ratio_-_2D4D.jpg\|thumb\|Androgen and Digit ratio (2D:4D]]		[[File:Finger_length_ratio_-_2D4D.jpg\|thumb\|Androgen and Digit ratio (2D:4D]]
	The ratio of 2nd and 4th finger (D, digit) length. This ratio has been suggested to relate to high fetal [[T#testosterone\|testosterone]] concentration (males have lower 2D:4D than females) and has been shown for several species.~~<ref><pubmed>~~16504142~~</pubmed></ref>~~ Although a study in mice has not shown the same correlation.~~<ref><pubmed>~~19495421~~</pubmed></ref>~~ There have been some suggestions that the ratio may also be an indicator of various neurological abnormalities.		The ratio of 2nd and 4th finger (D, digit) length. This ratio has been suggested to relate to high fetal [[T#testosterone\|testosterone]] concentration (males have lower 2D:4D than females) and has been shown for several species.{{#pmid:16504142\|PMID16504142}} Although a study in mice has not shown the same correlation.{{#pmid:19495421\|PMID19495421}} There have been some suggestions that the ratio may also be an indicator of various neurological abnormalities.

	'''To measure (2D:4D)''' - using your right hand palm up, measure the index finger (2) and ring finger (4) length from palm to tip. Dividing the index finger by the ring finger gives the 2D:4D ratio, average women ratio is 1, average men is 0.98.		'''To measure (2D:4D)''' - using your right hand palm up, measure the index finger (2) and ring finger (4) length from palm to tip. Dividing the index finger by the ring finger gives the 2D:4D ratio, average women ratio is 1, average men is 0.98.
Line 100:		Line 101:
	==Additional Images==		==Additional Images==

	{{~~Template:~~Glossary}}		{{Glossary}}

	{{~~Template:~~Footer}}		{{Footer}}

	[[Category:Endocrine]] [[Category:Gonad]]		[[Category:Endocrine]] [[Category:Gonad]]

Z8600021 at 00:33, 23 Mayıs 2017

2017-05-23T00:33:36Z

← Older revision		Revision as of 10:33, 23 Mayıs 2017
Line 11:		Line 11:


			{{Endocrine Links}}

	~~:{{Genital Links}}~~

	{{~~Endocrine~~ Links}}		{{Genital Links}}

	== Some Recent Findings ==		== Some Recent Findings ==

Z8600021 at 00:32, 23 Mayıs 2017

2017-05-23T00:32:20Z

← Older revision		Revision as of 10:32, 23 Mayıs 2017
Line 25:		Line 25:

	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
	! More recent papers		! More recent papers
	\|-		\|-
	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

Z8600021 at 01:09, 9 March 2016

2016-03-09T01:09:58Z

← Older revision		Revision as of 11:09, 9 March 2016
Line 54:		Line 54:

	==Male Hormone Levels==		==Male Hormone Levels==
			Testicular Leydig cells (interstitial cells) are the main source of testosterone in males.

	[[File:Male_testosterone_and_AMH_level_graph.jpg\|600px]]		[[File:Male_testosterone_and_AMH_level_graph.jpg\|600px]]

Z8600021 at 01:08, 9 March 2016

2016-03-09T01:08:01Z

← Older revision		Revision as of 11:08, 9 March 2016
Line 20:		Line 20:
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
			* '''Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes'''<ref name="PMID26929346"><pubmed>26929346</pubmed></ref> "Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. ... The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor β (TGF-β). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-β, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage."
	* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''<ref><pubmed>22238103</pubmed></ref> "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]		* '''Fetal Testosterone (FT) Influences Sexually Dimorphic Gray Matter in the Human Brain'''<ref><pubmed>22238103</pubmed></ref> "These results bridge a long-standing gap between human and nonhuman species by showing that fetal testosterone acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain." [[#Male Hormone Levels\|Male Hormone Levels]] \| [[Neural System Development]]
	\|}		\|}