Effect of Hypoglycemic Drugs on Kisspeptin Expression in the Hypothalamic Arcuate Nucleus of PCOS Rats.
PCOS
acarbose
kisspeptin
metformin
pioglitazone
polycystic ovary syndrome
Journal
Diabetes, metabolic syndrome and obesity : targets and therapy
ISSN: 1178-7007
Titre abrégé: Diabetes Metab Syndr Obes
Pays: New Zealand
ID NLM: 101515585
Informations de publication
Date de publication:
2023
2023
Historique:
received:
17
06
2023
accepted:
23
08
2023
medline:
13
9
2023
pubmed:
13
9
2023
entrez:
13
9
2023
Statut:
epublish
Résumé
To investigate the change in hypothalamic kisspeptin-1 (Kiss1) expression during the development of polycystic ovary syndrome (PCOS) and hypoglycemic drug intervention. Letrozole lavage was used to construct a polycystic ovary rat model. After successful modeling, we treated PCOS rats with metformin, pioglitazone, and acarbose, and we then observed changes in weight, estrus, glucose tolerance, insulin resistance, sex hormones, and hypothalamic kiss1 expression. PCOS rats exhibited increased body weight, abnormal estrous cycle, impaired glucose tolerance, insulin resistance, increased testosterone level, increased luteinizing hormone level, and increased Kiss1 expression in the hypothalamus. However, intervention with metformin, pioglitazone, and acarbose improved the reproductive and metabolic disorders as well as reduced hypothalamic Kiss1 expression. The expression of hypothalamic Kiss1 may play an important role in the pathogenesis of PCOS. Metformin, pioglitazone, and acarbose may reduce the expression of hypothalamic Kiss1 by improving insulin resistance, thereby improving reproductive and metabolic disorders in PCOS rats.
Sections du résumé
Background
UNASSIGNED
To investigate the change in hypothalamic kisspeptin-1 (Kiss1) expression during the development of polycystic ovary syndrome (PCOS) and hypoglycemic drug intervention.
Methods
UNASSIGNED
Letrozole lavage was used to construct a polycystic ovary rat model. After successful modeling, we treated PCOS rats with metformin, pioglitazone, and acarbose, and we then observed changes in weight, estrus, glucose tolerance, insulin resistance, sex hormones, and hypothalamic kiss1 expression.
Results
UNASSIGNED
PCOS rats exhibited increased body weight, abnormal estrous cycle, impaired glucose tolerance, insulin resistance, increased testosterone level, increased luteinizing hormone level, and increased Kiss1 expression in the hypothalamus. However, intervention with metformin, pioglitazone, and acarbose improved the reproductive and metabolic disorders as well as reduced hypothalamic Kiss1 expression.
Conclusion
UNASSIGNED
The expression of hypothalamic Kiss1 may play an important role in the pathogenesis of PCOS. Metformin, pioglitazone, and acarbose may reduce the expression of hypothalamic Kiss1 by improving insulin resistance, thereby improving reproductive and metabolic disorders in PCOS rats.
Identifiants
pubmed: 37701721
doi: 10.2147/DMSO.S421911
pii: 421911
pmc: PMC10494929
doi:
Types de publication
Journal Article
Langues
eng
Pagination
2717-2732Informations de copyright
© 2023 Zheng et al.
Déclaration de conflit d'intérêts
Pingping Zheng, Yating Lu and You Tang are co-first authors for this study. The authors declare that they have no competing interests for this work.
Références
Nat Rev Endocrinol. 2018 May;14(5):270-284
pubmed: 29569621
Nat Rev Endocrinol. 2020 Aug;16(8):407-420
pubmed: 32427949
Reprod Med Biol. 2021 Oct 07;21(1):e12419
pubmed: 34934400
J Endocrinol. 2015 Aug;226(2):T41-54
pubmed: 25901041
Proc Natl Acad Sci U S A. 2018 Nov 6;115(45):E10758-E10767
pubmed: 30348767
Endocr J. 2017 Jan 30;64(1):7-14
pubmed: 27665725
Eur J Endocrinol. 2011 Feb;164(2):197-203
pubmed: 21059865
Reprod Sci. 2020 Feb;27(2):455-460
pubmed: 31919796
Hum Reprod. 2010 Feb;25(2):544-51
pubmed: 19910321
Biol Reprod. 2015 Sep;93(3):69
pubmed: 26203175
Hum Reprod. 2005 Sep;20(9):2396-401
pubmed: 16006454
Arch Med Res. 2018 Apr;49(3):154-163
pubmed: 30104075
Environ Toxicol Pharmacol. 2019 Feb;66:43-54
pubmed: 30597379
Reprod Med Biol. 2021 Sep 20;21(1):e12414
pubmed: 34934398
Cochrane Database Syst Rev. 2017 Nov 29;11:CD003053
pubmed: 29183107
Arch Med Res. 2004 Mar-Apr;35(2):103-8
pubmed: 15010188
Brain Res. 2012 Jul 27;1467:1-9
pubmed: 22668987
Sheng Li Xue Bao. 2020 Feb 25;72(1):125-132
pubmed: 32099990
Gynecol Endocrinol. 2016;32(2):136-8
pubmed: 26440054
Semin Reprod Med. 2019 May;37(3):141-146
pubmed: 31869842
Cells. 2022 Oct 06;11(19):
pubmed: 36231110
Clin Chim Acta. 2020 Mar;502:214-221
pubmed: 31733195
Nat Rev Dis Primers. 2016 Aug 11;2:16057
pubmed: 27510637
Endocrinology. 2020 Apr 1;161(4):
pubmed: 32031594
J Endocrinol. 2018 Sep;238(3):R173-R183
pubmed: 30042117
World J Diabetes. 2021 May 15;12(5):616-629
pubmed: 33995849
Reprod Biol. 2016 Mar;16(1):53-60
pubmed: 26952754
PLoS One. 2013 Nov 18;8(11):e79697
pubmed: 24260283
Fertil Steril. 2008 Oct;90(4):1144-8
pubmed: 18377903
J Steroid Biochem Mol Biol. 2018 Sep;182:27-36
pubmed: 29678491
Endocrinology. 2019 Mar 1;160(3):699-715
pubmed: 30657917
Reprod Biomed Online. 2019 Oct;39(4):685-697
pubmed: 31515170
J Clin Invest. 2020 Dec 1;130(12):6739-6753
pubmed: 33196464
J Endocrinol. 2015 Nov;227(2):105-15
pubmed: 26446276
Arch Gynecol Obstet. 2017 Oct;296(4):661-677
pubmed: 28770353
Endocr Rev. 2012 Dec;33(6):981-1030
pubmed: 23065822
Endocrinology. 2022 Feb 1;163(2):
pubmed: 34953135
Clin Endocrinol (Oxf). 2022 Mar;96(3):371-394
pubmed: 34713480
Exp Ther Med. 2019 May;17(5):4013-4022
pubmed: 30988783