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positive feedback loop. If conception occurs, the placenta will take over the secretion of progesterone; therefore the mother cannot ovulate again. If conception does not occur, decreasing excretion of progesterone will allow the hypothalamus to restart secretion of GnRH. These hormone levels also control the uterine (menstrual) cycle causing the proliferation phase in preparation for ovulation, the secretory phase after ovulation, and menstruation when conception does not occur. The activation of the HPG axis in both males and females during puberty also causes individuals to acquire secondary sex characteristics.
31:
402:, which mimic biologically derived progesterone. The synthetic progestin prevents the hypothalamus from releasing GnRH and the pituitary from releasing LH and FSH; therefore it prevents the ovarian cycle from entering the menstrual phase and prevents follicle development and ovulation. Also as a result, many of the side effects are similar to the symptoms of pregnancy. Alzheimer's has been shown to have a hormonal component, which could possibly be used as a method to prevent the disease.
511:
525:
325:. These physical differences lead to differences in behavior. While GnRH has not been shown to have any direct influence on regulating brain structure and function, gonadotropins, sex steroids, and activin have been shown to have such effects. It is thought that FSH may have an important role in brain development and differentiation.
1154:
Baird, D. T.; Balen, A.; Escobar-Morreale, H. F.; Evers, J. L. H.; Fauser, B. C. J. M.; Franks, S.; Glasier, A.; Homburg, R.; La
Vecchia, C.; Devroey, P.; Diedrich, K.; Fraser, L.; Gianaroli, L.; Liebaers, I.; Sunde, A.; Tapanainen, J. S.; Tarlatzis, B.; Van Steirteghem, A.; Veiga, A.; Crosignani, P.
385:
cause male pseudohermaphroditism. In females mutations would have analogous effects. Hormone replacement can be used to initiate puberty and continue if the gene mutation occurs in the gene coding for the hormone. Chromosomal mutations tend to affect the androgen production rather than the HPG axis.
384:
For example, the male mutation of the GnRH coding gene could result in hypogonadotrophic hypogonadism. A mutation that cause a gain of function for LH receptor can result in a condition known as testotoxicosis, which cause puberty to occur between ages 2–3 years. Loss of function of LH receptors can
249:
loop between estrogen and luteinizing hormone help to prepare the follicle in the ovary and the uterus for ovulation and implantation. When the egg is released, the empty follicle sac begins to produce progesterone to inhibit the hypothalamus and the anterior pituitary thus stopping the estrogen-LH
120:
organisms (e.g. fish, reptiles, amphibians, birds), the HPG axis is commonly referred to as the hypothalamus-pituitary-gonadal-liver axis (HPGL-axis) in females. Many egg-yolk and chorionic proteins are synthesized heterologously in the liver, which are necessary for ovocyte growth and development.
498:
The HPG axis is highly conserved in the animal kingdom. While reproductive patterns may vary, the physical components and control mechanisms remain the same. The same hormones are used with some minor evolutionary modifications. Much of the research is done on animal models, because they mimic so
380:
Genetic mutations and chromosomal abnormalities are two sources of HPG axis alteration. Single mutations usually lead to changes in binding ability of the hormone and receptor leading to inactivation or over activation. These mutations can occur in the genes coding for GnRH, LH, and FSH or their
302:. The cause of the decreased testosterone is unclear and a current topic of research. Post-pubertal hypogonadism results in progressive muscle mass decrease, increase in visceral fat mass, loss of libido, impotence, decreased attention, increased risk of fractures, and abnormal sperm production.
265:
binding. LH binds to the interstitial cells, causing them to secrete testosterone. Testosterone is required for normal spermatogenesis and inhibits the hypothalamus. Inhibin is produced by the spermatogenic cells, which, also through inactivating activin, inhibits the hypothalamus. After puberty
485:
Environment can have large impact on the HPG axis. For example, women with eating disorders tend to have oligomenorrhea and secondary amenorrhea. Starvation from anorexia nervosa or bulimia causes the HPG axis to deactivate causing women's ovarian and uterine cycles to stop. Stress, physical
77:
The HPG axis plays a critical part in the development and regulation of a number of the body's systems, such as the reproductive and immune systems. Fluctuations in this axis cause changes in the hormones produced by each gland and have various local and systemic effects on the body.
332:. This helps create synaptogenesis by promoting neurite development and migration. Activin promotes neural plasticity throughout the lifespan and regulates the neurotransmitters of peripheral neurons. Environment can also affect hormones and behavior interaction.
397:
administration. Although often described as preventing pregnancy by mimicking the pregnancy state, hormonal birth control is effective because it works on the HPG axis to mimic the luteal phase of a woman's cycle. The primary active ingredients are synthetic
274:
The activation and deactivation of the HPG axis also helps to regulate life cycles. At birth FSH and LH levels are elevated, and females also have a lifetime supply of primary oocytes. These levels decrease and remain low through childhood. During
499:
well the control mechanism of humans. It is important to remember humans are the only species to hide their fertile period, but this effect is a difference in the effect of the hormones rather than a difference in the HPG axis.
291:. This deregulation is caused mainly by the lack of oocytes that normally produce estrogen to create the positive feedback loop. Over several years, the activity the HPG axis decreases and women are no longer fertile.
1384:
Sower SA, Freamat M, Kavanaugh SI (March 2009). "The origins of the vertebrate hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-thyroid (HPT) endocrine systems: new insights from lampreys".
287:
and testosterone causes physiological and psychological changes. Once activated, the HPG axis continues to function in men for the rest of their life but becomes deregulated in women, leading to
704:"Identification of a regulatory loop for the synthesis of neurosteroids: a steroidogenic acute regulatory protein-dependent mechanism involving hypothalamic-pituitary-gonadal axis receptors"
205:. Only small amounts of estrogen are secreted in males. Recent research has shown that a neurosteroid axis exists, which helps the cortex to regulate the hypothalamus's production of GnRH.
1602:
197:, which is also produced in all body tissue, inhibits activin and gives the rest of the body more control over the axis. In males LH stimulates the interstitial cells located in the
1235:"A luteinizing hormone receptor intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E epsilon4 allele"
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as breast cancer management, to prevent the body's formation of estrogen which may stimulate breast cancer cells. This is generally done by continuous administration of
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exercise, and weight loss have been correlated with oligomenorrhea and secondary amenorrhea. Similarly environmental factors can also affect men such as stress causing
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1469:
1464:
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Vadakkadath
Meethal S, Atwood CS (February 2005). "The role of hypothalamic-pituitary-gonadal hormones in the normal structure and functioning of the brain".
543:
538:
133:
129:
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Wiksten-Almströmer M, Hirschberg AL, Hagenfeldt K (2007). "Menstrual disorders and associated factors among adolescent girls visiting a youth clinic".
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also affect behavior, because sex steroids affect the brains structure and functioning. During development, hormones help determine how neurons
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One of the most important functions of the HPG axis is to regulate reproduction by controlling the uterine and ovarian cycles. In females, the
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865:
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490:. Prenatal exposure to alcohol can affect the hormones regulating fetal development resulting in foetal alcohol spectrum disorder.
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These two hormones play an important role in communicating to the gonads. In females FSH and LH act primarily to activate the
30:
221:
82:
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In males, the production of GnRH, LH, and FSH are similar, but the effects of these hormones are different. FSH stimulates
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in order to decrease negative feedback on the pituitary gland, resulting in an increase in FSH with the aim of increasing
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receptors. Depending on which hormone and receptor are unable to bind different effects occur but all alter the HPG axis.
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102:
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1329:"Prenatal alcohol exposure: fetal programming, the hypothalamic-pituitary-adrenal axis and sex differences in outcome"
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159:
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Disorders of the hypothalamic–pituitary–gonadal axis are classified by the World Health
Organization (WHO) as:
258:
702:
Meethal SV, Liu T, Chan HW, Ginsburg E, Wilson AC, Gray DN, Bowen RL, Vonderhaar BK, Atwood CS (August 2009).
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1155:
G.; Evers, J. L. H. (2012). "Health and fertility in World Health
Organization group 2 anovulatory women".
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is located in the brain and secretes GnRH. GnRH travels down the anterior portion of the pituitary via the
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182:
367:. WHO group II is the most common cause of ovulation disorders, and the most common causative member is
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HPG regulation in males, with the inhibin/activin system playing a similar role on GnRH-producing cells
166:. In response to GnRH stimulation these cells produce LH and FSH, which travel into the blood stream.
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Although males remain fertile until death, the activity of the HPG axis decreases. As males age, the
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98:
445:, in order to prevent the spontaneous ovulation of ovarian follicles before they can be harvested.
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the HPG axis is activated by the secretions of estrogen from the ovaries or testosterone from the
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Haasl RJ, Ahmadi MR, Meethal SV, Gleason CE, Johnson SC, Asthana S, Bowen RL, Atwood CS (2008).
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axes are three pathways in which the hypothalamus and pituitary direct neuroendocrine function.
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193:, which is a peripherally produced hormone that positively stimulates GnRH-producing cells.
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Concept of regarding the hypothalamus, pituitary gland and gonadal glands as a single entity
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94:
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55:
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Hines M (July 1982). "Prenatal gonadal hormones and sex differences in human behavior".
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Veldhuis JD, Keenan DM, Liu PY, Iranmanesh A, Takahashi PY, Nehra AX (February 2009).
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1078:"Genetic, epigenetic and environmental impact on sex differences in social behavior"
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begin to produce less testosterone, leading to a condition known as post-pubertal
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886:"The aging male hypothalamic-pituitary-gonadal axis: pulsatility and feedback"
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Millar RP, Lu ZL, Pawson AJ, Flanagan CA, Morgan K, Maudsley SR (April 2004).
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find it convenient and descriptive to speak of them as a single system.
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794:"The kisspeptin-GnRH pathway in human reproductive health and disease"
753:"The relationship between gut and adipose hormones, and reproduction"
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The axis controls development, reproduction, and aging in animals.
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were a single entity. Because these glands often act in concert,
860:. San Francisco: Pearson Benjamin Cummings. pp. 1090–1110.
620:"Hypothalamic control of anterior pituitary function: a history"
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Isidori AM, Giannetta E, Lenzi A (2008). "Male hypogonadism".
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Shepard KN, Michopoulos V, Toufexis DJ, Wilson ME (May 2009).
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utilizing sex hormones approach the problem in a similar way.
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Weinberg J, Sliwowska JH, Lan N, Hellemans KG (April 2008).
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Oxford handbook of reproductive medicine and family planning
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Wibral M, Dohmen T, Klingmüller D, Weber B, Falk A (2012).
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by inhibiting the production of GnRH in the hypothalamus.
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Skorupskaite, K.; George, J. T.; Anderson, R. A. (2014).
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Comninos, A. N.; Jayasena, C. N.; Dhillo, W. S. (2013).
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and binds to receptors on the secretory cells of the
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Guillebaud, John; Enda McVeigh; Roy
Homburg (2008).
935:"The role of the brain in female reproductive aging"
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to produce estrogen and inhibin and to regulate the
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1019:"Testosterone Administration Reduces Lying in Men"
853:
266:these hormones levels remain relatively constant.
328:Testosterone levels have been shown to relate to
201:to produce testosterone, and FSH plays a role in
1603:Gonadotropin-releasing hormone and gonadotropins
473:. It is the main initial medical treatment for
121:Examples of such necessary liver proteins are
48:hypothalamic–pituitary–ovarian/testicular axis
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8:
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457:is usually initially performed by giving an
852:Katja Hoehn; Marieb, Elaine Nicpon (2007).
1547:Reproductive endocrinology and infertility
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579:"Gonadotropin-releasing hormone receptors"
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417:, such as in the following applications
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409:The HPG axis can also be suppressed by
1485:Hypothalamic–pituitary–prolactin axis
7:
1490:Hypothalamic–neurohypophyseal system
1133:. Oxford : Oxford University Press.
549:Hypothalamic–neurohypophyseal system
1475:Hypothalamic–pituitary–gonadal axis
1470:Hypothalamic–pituitary–adrenal axis
1465:Hypothalamic–pituitary–thyroid axis
933:Downs JL, Wise PM (February 2009).
544:Hypothalamic–pituitary–thyroid axis
539:Hypothalamic–pituitary–adrenal axis
436:controlled ovarian hyperstimulation
40:hypothalamic–pituitary–gonadal axis
393:The HPG axis can be suppressed by
365:Hypothalamic–pituitary dysfunction
25:
1345:10.1111/j.1365-2826.2008.01669.x
720:10.1111/j.1471-4159.2009.06192.x
637:10.1111/j.1365-2826.2008.01718.x
523:
509:
413:or continuous administration of
232:also influences GnRH secretion.
856:Human anatomy & physiology
355:Hypothalamic–pituitary failure
306:Sexual dimorphism and behavior
222:gonadotropin-releasing hormone
105:(FSH), and the gonads produce
93:. The anterior portion of the
83:Gonadotropin-releasing hormone
1:
1608:Human female endocrine system
1094:10.1016/j.physbeh.2009.02.016
216:have stimulatory effects and
1044:10.1371/journal.pone.0046774
103:follicle-stimulating hormone
85:(GnRH) is secreted from the
1399:10.1016/j.ygcen.2008.11.023
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559:Reproductive endocrinology
224:(GnRH) secretion from the
220:has inhibitory effects on
1298:10.1080/00016340601034970
1286:Acta Obstet Gynecol Scand
1204:10.1007/s11102-008-0111-9
1157:Human Reproduction Update
996:10.1037/0033-2909.92.1.56
951:10.1016/j.mce.2008.11.012
902:10.1016/j.mce.2008.09.005
798:Human Reproduction Update
757:Human Reproduction Update
681:10.1007/s00018-004-4381-3
369:polycystic ovary syndrome
160:hypophyseal portal system
1542:Psychoneuroendocrinology
1495:Renin–angiotensin system
618:Charlton H (June 2008).
259:androgen-binding protein
1537:Pediatric endocrinology
140:Location and regulation
91:GnRH-expressing neurons
62:as if these individual
1511:Blood sugar regulation
1252:10.1186/1471-2350-9-37
395:hormonal birth control
183:negative feedback loop
151:
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1563:Wolff–Chaikoff effect
1387:Gen. Comp. Endocrinol
1169:10.1093/humupd/dms019
939:Mol. Cell. Endocrinol
890:Mol. Cell. Endocrinol
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770:10.1093/humupd/dmt033
432:Ovulation suppression
283:. This activation of
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596:10.1210/er.2003-0002
46:, also known as the
1035:2012PLoSO...746774W
669:Cell. Mol. Life Sci
494:Comparative anatomy
481:Environment factors
455:Ovulation induction
422:Ovarian suppression
404:Male contraceptives
361:ovulation disorders
351:ovulation disorders
255:sustentacular cells
181:. Estrogen forms a
99:luteinizing hormone
1593:Neuroendocrinology
1567:Jod-Basedow effect
1532:Neuroendocrinology
1516:Calcium metabolism
1458:Regulatory systems
1333:J. Neuroendocrinol
624:J. Neuroendocrinol
554:Neuroendocrinology
336:Clinical relevance
330:prosocial behavior
323:sexual dimorphisms
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878:
874:
869:
863:
858:
857:
848:
846:
842:
837:
833:
828:
823:
819:
815:
811:
807:
803:
799:
795:
788:
785:
780:
776:
771:
766:
763:(2): 153–74.
762:
758:
754:
747:
744:
739:
735:
730:
725:
721:
717:
713:
709:
705:
698:
695:
690:
686:
682:
678:
675:(3): 257–70.
674:
670:
663:
660:
655:
651:
647:
643:
638:
633:
629:
625:
621:
614:
611:
606:
602:
597:
592:
589:(2): 235–75.
588:
584:
580:
573:
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564:
560:
557:
555:
552:
550:
547:
545:
542:
540:
537:
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518:
512:
507:
502:
500:
493:
491:
489:
480:
478:
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468:
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449:
444:
443:fertilization
442:
437:
433:
430:
427:
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419:
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412:
407:
405:
401:
396:
388:
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375:
370:
366:
362:
358:
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352:
348:
347:
346:
340:
335:
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331:
326:
324:
321:to result in
320:
316:
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305:
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292:
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278:
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208:In addition,
206:
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192:
188:
184:
180:
179:ovarian cycle
176:
172:
167:
165:
161:
157:
148:
144:
139:
137:
135:
131:
126:
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119:
114:
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73:
69:
68:physiologists
65:
61:
57:
53:
49:
45:
41:
32:
19:
1474:
1390:
1386:
1379:
1336:
1332:
1322:
1292:(1): 65–72.
1289:
1285:
1279:
1242:
1238:
1228:
1195:
1191:
1185:
1160:
1156:
1149:
1130:
1120:
1085:
1081:
1071:
1026:
1022:
1012:
990:(1): 56–80.
987:
984:Psychol Bull
983:
977:
942:
938:
928:
896:(1): 14–22.
893:
889:
855:
801:
797:
787:
760:
756:
746:
711:
708:J. Neurochem
707:
697:
672:
668:
662:
630:(6): 641–6.
627:
623:
613:
586:
582:
572:
497:
484:
459:antiestrogen
453:
440:
426:GnRH agonist
415:GnRH agonist
408:
392:
383:
379:
364:
354:
344:
327:
311:Sex steroids
309:
300:hypogonadism
293:
273:
263:testosterone
252:
244:
241:Reproduction
226:hypothalamus
207:
168:
156:hypothalamus
153:
143:
127:
123:vitellogenin
115:
111:testosterone
87:hypothalamus
80:
76:
52:hypothalamus
47:
43:
39:
37:
1393:(1): 20–9.
945:(1): 32–8.
583:Endocr. Rev
475:anovulation
450:Stimulation
434:as part of
389:Suppression
257:to release
195:Follistatin
132:, HPG, and
1587:Categories
1504:Metabolism
1447:Physiology
565:References
400:progestins
270:Life cycle
230:Kisspeptin
1192:Pituitary
818:1355-4786
488:impotence
467:letrozole
341:Disorders
289:menopause
199:testicles
118:oviparous
101:(LH) and
97:produces
1407:19084529
1363:18266938
1314:24096186
1306:17230292
1271:18439297
1220:20813241
1212:18404386
1177:22611175
1112:19250945
1063:23071635
1023:PLOS ONE
969:19063938
920:18838102
836:24615662
779:24173881
738:19493163
689:15723162
654:16955603
646:18601683
605:15082521
503:See also
461:such as
441:in vitro
285:estrogen
236:Function
107:estrogen
44:HPG axis
18:HPG axis
1449:of the
1371:4574957
1354:8942074
1262:2396156
1125:Page 54
1103:2670935
1054:3468628
1031:Bibcode
1004:7134329
960:2692385
911:2662347
827:4063702
729:2789665
371:(PCOS).
319:migrate
315:synapse
277:puberty
218:ghrelin
214:insulin
191:activin
187:Inhibin
171:ovaries
1525:Fields
1405:
1369:
1361:
1351:
1312:
1304:
1269:
1259:
1245:: 37.
1218:
1210:
1175:
1137:
1110:
1100:
1061:
1051:
1002:
967:
957:
918:
908:
864:
834:
824:
816:
777:
736:
726:
687:
652:
644:
603:
296:testes
281:testes
210:leptin
58:, and
1556:Other
1367:S2CID
1310:S2CID
1216:S2CID
650:S2CID
1403:PMID
1359:PMID
1302:PMID
1267:PMID
1208:PMID
1173:PMID
1135:ISBN
1127:in:
1108:PMID
1059:PMID
1000:PMID
965:PMID
916:PMID
862:ISBN
832:PMID
814:ISSN
775:PMID
734:PMID
685:PMID
642:PMID
601:PMID
317:and
212:and
177:and
154:The
128:The
109:and
70:and
38:The
1395:doi
1391:161
1349:PMC
1341:doi
1294:doi
1257:PMC
1247:doi
1200:doi
1165:doi
1098:PMC
1090:doi
1049:PMC
1039:doi
992:doi
955:PMC
947:doi
943:299
906:PMC
898:doi
894:299
822:PMC
806:doi
765:doi
724:PMC
716:doi
712:110
677:doi
632:doi
591:doi
465:or
438:in
134:HPT
130:HPA
116:In
89:by
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1401:.
1389:.
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1357:.
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1308:.
1300:.
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1255:.
1241:.
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1196:11
1194:.
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1161:18
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1096:.
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1084:.
1080:.
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1047:.
1037:.
1025:.
1021:.
998:.
988:92
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963:.
953:.
941:.
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876:^
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830:.
820:.
812:.
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673:62
671:.
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628:20
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587:25
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581:.
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353::
228:.
113:.
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1273:.
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1222:.
1202::
1179:.
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1143:.
1114:.
1092::
1065:.
1041::
1033::
1027:7
1006:.
994::
971:.
949::
922:.
900::
870:.
838:.
808::
781:.
767::
740:.
718::
691:.
679::
656:.
634::
607:.
593::
428:.
42:(
20:)
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