The ovarian reserve as target of insulin/IGF and ROS in metabolic disorder-dependent ovarian dysfunctions.
ROS
female infertility
insulin/IGF
metabolic disorders
ovarian reserve
Journal
Reproduction & fertility
ISSN: 2633-8386
Titre abrégé: Reprod Fertil
Pays: England
ID NLM: 101778727
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
received:
15
07
2021
accepted:
17
08
2021
entrez:
4
2
2022
pubmed:
5
2
2022
medline:
5
2
2022
Statut:
epublish
Résumé
It is known for a long time that metabolic disorders can cause ovarian dysfunctions and affect a woman's fertility either by direct targeting follicular cells and/or the oocytes or by indirect interference with the pituitary-hypothalamic axis, resulting in dysfunctional oogenesis. Such disorders may also influence the efficiency of the embryo implantation and the quality of the embryo with permanent effects on the fertility and health of the offspring. Thanks to the expanding knowledge on the molecular mechanisms governing oogenesis and folliculogenesis in mammals, we are beginning to understand how such disorders can negatively affect this process and consequently fertility in women. In the present review, we point out and discuss how the disturbance of insulin/IGF-dependent signalling and increased reactive oxygen species (ROS) level in the ovary typically associated to metabolic disorders such as type II diabetes and obesity can dysregulate the dynamics of the ovarian reserve and/or impair the survival and competence of the oocytes. In women, a progressive decline and depletion of the primary ovary reserve, which represents the reserve of immature eggs, are a challenging condition in the field of reproductive medicine. This decline, occurring physiological with age, is the main determinant of the age at the onset of menopause. Concomitant with the reduction in their number, the quality of the eggs also decreases with age. Metabolic disorders such as diabetes and obesity can cause ovarian dysfunctions and affect a woman's fertility mainly by direct targeting the egg stockpile or by indirect interference with the production of reproductive hormones. Here, we report up-to-date data and discuss results about how disturbance of insulin-dependent signalling and increased oxidative stress in the ovary, usually associated to metabolic disorders, can dysregulate the dynamics of the primary ovary reserve and/or impair the survival and quality of the eggs.
Identifiants
pubmed: 35118400
doi: 10.1530/RAF-21-0038
pii: RAF-21-0038
pmc: PMC8801032
doi:
Substances chimiques
Insulin
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Review
Langues
eng
Pagination
R103-R112Informations de copyright
© The authors.
Références
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8060-5
pubmed: 12048244
Endocr Rev. 2015 Feb;36(1):1-24
pubmed: 25202833
Eur J Obstet Gynecol Reprod Biol. 1994 May 31;55(1):29-30
pubmed: 7958135
J Cell Physiol. 2019 Feb;234(2):1578-1587
pubmed: 30078193
Reproduction. 2006 Mar;131(3):525-32
pubmed: 16514195
Fertil Steril. 2008 Oct;90(4 Suppl):1333-9
pubmed: 18054353
Trends Endocrinol Metab. 2010 Feb;21(2):96-103
pubmed: 19913438
Hum Mol Genet. 2009 Aug 1;18(15):2813-24
pubmed: 19423553
Acta Histochem. 2015 May-Jun;117(4-5):468-76
pubmed: 25724694
Reproduction. 2019 Sep;158(3):R79-R90
pubmed: 30999278
Mol Endocrinol. 1996 Jul;10(7):903-18
pubmed: 8813730
Mol Endocrinol. 2014 Jan;28(1):138-50
pubmed: 24243489
Proc Natl Acad Sci U S A. 2013 Oct 22;110(43):17474-9
pubmed: 24082083
Endocrinology. 2012 Jan;153(1):404-16
pubmed: 22128018
Hum Reprod Update. 2019 Nov 5;25(6):673-693
pubmed: 31600388
Biol Reprod. 2000 Dec;63(6):1669-75
pubmed: 11090434
J Hematol Oncol. 2020 Jun 16;13(1):77
pubmed: 32546241
Histochem Cell Biol. 2010 Jul;134(1):75-82
pubmed: 20495820
Braz J Med Biol Res. 2010 Aug;43(8):728-36
pubmed: 20640385
Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10280-4
pubmed: 20479243
Dev Biol. 1997 Apr 15;184(2):333-42
pubmed: 9133439
Reprod Fertil Dev. 2018 Oct;30(11):1503-1513
pubmed: 29843892
J Assist Reprod Genet. 2011 Jan;28(1):3-6
pubmed: 20872066
Trends Biochem Sci. 2013 Mar;38(3):160-7
pubmed: 23394938
Nat Cell Biol. 2012 Dec;14(12):1322-9
pubmed: 23143395
J Assist Reprod Genet. 2013 Oct;30(10):1279-88
pubmed: 23934019
Oxid Med Cell Longev. 2017;2017:4371714
pubmed: 29147461
Hum Mol Genet. 2010 Feb 1;19(3):397-410
pubmed: 19843540
Growth Horm IGF Res. 2000 Jun;10(3):111-7
pubmed: 10942631
Menopause. 2017 Mar;24(3):345-351
pubmed: 27749734
Oxid Med Cell Longev. 2016;2016:3565127
pubmed: 27247702
FASEB J. 2015 Jun;29(6):2423-30
pubmed: 25690654
PLoS One. 2009 Jul 09;4(7):e6186
pubmed: 19587782
Mol Cell Endocrinol. 2012 Jul 6;358(1):18-26
pubmed: 22366471
Front Endocrinol (Lausanne). 2019 Jun 07;10:346
pubmed: 31231310
PLoS One. 2011;6(5):e20087
pubmed: 21637711
Biol Reprod. 2016 Dec;95(6):129
pubmed: 27683265
Genetics. 2020 Jun;215(2):373-378
pubmed: 32273296
Biol Reprod. 2015 Jul;93(1):22
pubmed: 26040669
Cell Physiol Biochem. 2015;35(3):957-68
pubmed: 25659841
PLoS One. 2015 May 29;10(5):e0127786
pubmed: 26024525
Theriogenology. 2009 May;71(8):1193-208
pubmed: 19193432
Science. 2008 Feb 1;319(5863):611-3
pubmed: 18239123
Acta Biochim Biophys Sin (Shanghai). 2015 Jan;47(1):2-9
pubmed: 25476206
PLoS One. 2019 Apr 11;14(4):e0215007
pubmed: 30973884
Vitam Horm. 2014;94:99-127
pubmed: 24388188
Proc Natl Acad Sci U S A. 2019 Jun 18;116(25):12321-12326
pubmed: 31147464
Endocrinology. 2005 Feb;146(2):941-9
pubmed: 15539559
Annu Rev Genet. 2018 Nov 23;52:65-87
pubmed: 30183404
Curr Biol. 2014 Nov 3;24(21):2501-8
pubmed: 25438940
Cell. 2017 Apr 6;169(2):361-371
pubmed: 28388417
Hum Reprod Update. 2018 May 1;24(3):267-289
pubmed: 29447380
J Clin Endocrinol Metab. 2016 Oct;101(10):3568-3570
pubmed: 27702318
Mol Hum Reprod. 2014 Aug;20(8):736-44
pubmed: 24830779
J Reprod Immunol. 2011 Mar;88(2):142-8
pubmed: 21333359
Nat Med. 2013 May;19(5):557-66
pubmed: 23652116
FASEB J. 2019 Sep;33(9):10049-10064
pubmed: 31199671
Mol Hum Reprod. 2000 Aug;6(8):694-8
pubmed: 10908278
PLoS Genet. 2020 Nov 18;16(11):e1009067
pubmed: 33206637