Main Article Content
Abstract
We aim to evaluate the efficacy and optimal dose of orally administered DHEA in the PCOS mice model by assessing their ovarian morphology and serum FSH, LH, and testosterone levels. Female C57BL/6 mice were divided into a control group (n=5, received daily injections of 0.2 ml sesame oil) and an experimental group, which was further classified into 1) D-45 group (n=5), 2) D-60 (n=5), and 3) D-90 group (n=5) that were treated with 45, 60, and 90 mg/Kg body weight of oral DHEA. After modelling, mice in the control group had a regular estrous cycle, while mice in all experimental groups had a disturbed estrous cycle. Ovarian histology showed several growing follicles and some corpora lutea (CL) in the control, D-60, and D-90 groups. However, some large antral follicles and decreased CL were observed in the D-45 group. Serum FSH was significantly lower in the D-45 group than in the control group (3.73 ± 0.12 vs. 5.28 ± 0.31 mIU/mL, P<0.01), but D-60 and D-90 groups had a similar FSH level to the control group (P>0.05). The serum level of LH and testosterone were significantly elevated in the D-45 group than in the control group (2.52 ± 0.43 vs. 1.30 ± 0.33 mIU/mL, P<0.01 and 1.80 ± 0.32 vs. 1.24 ± 0.23 ng/mL, P<0.01, respectively). Still, the level of LH and testosterone in the D-60 and the D-90 groups was comparable to the control group (P>0.05). Our study suggests that oral administration of DHEA is efficacious in establishing PCOS-like phenotype in mice with the suggested optimal dosage of 45 mg/Kg body weight.
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References
- Azziz R. 2006. Diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature. Journal of Clinical Endocrinology and Metabolism. 91:781–785. DOI: 10.1210/jc.2005-2153
- Deswal R, Narwal V, Dang A, Pundir CS. 2020. The prevalence of polycystic ovary syndrome: a brief systematic review. Journal of Human Reproductive Science 13: 261–271. DOI: 10.4103/jhrs.JHRS_95_18
- Fahed G, Aoun L, Zerdan MB, Allam S, Zerdan MB, Bouferraa Y, Assi HI. 2022. Metabolic syndrome: updates on pathophysiology and management in 2021. International Journal of Molecular Sciences 23: 786. DOI: 10.3390/ijms23020786
- Fu L, Xie N, Qu F, Zhou J, Wang F. 2023. The association between polycystic ovary syndrome and metabolic syndrome in adolescents: a systematic review and meta-analysis. Reproductive Sciences 30: 28. DOI: 10.1007/s43032-022-00864-8
- Karee M, Gundabattula SR, Sashi L, Boorugu H. 2020. Prevalence of metabolic syndrome in women with polycystic ovary syndrome and the factors associated : A cross sectional study at a tertiary care center in Hyderabad, south-eastern India. Diabetes and Metabolic Syndrom 14:583–587. DOI: 10.1016/j.dsx.2020.05.006
- Li Y, Zheng Q, Sun D, Cui X, Chen S, Bulbul A, Liu S, Yan Q. 2019. Dehydroepiandrosterone stimulates inflammation and impairs ovarian functions of polycystic ovary syndrome. Journal of Cellular Physiology 234: 7435–7447. DOI: 10.1002/jcp.27501
- Lorincz CE, Börzsei D, Hoffmann A, Varga C, Szabó R. 2024. Mechanisms and target parameters in relation to polycystic ovary syndrome and physical exercise : focus on the master triad of hormonal changes, oxidative stress, and inflammation. Biomedicines 12: 560. DOI: 10.3390/biomedicines12030560
- Osuka S, Nakanishi N, Murase T, Nakamura T, Goto M, Iwase A, Kikkawa F. 2018. Animal models of polycystic ovary syndrome: A review of hormone‐induced rodent models focused on hypothalamus‐pituitary‐ovary axis and neuropeptides. Reproductive Medicine and Biology 18: 151–160. DOI: 10.1002/rmb2.12262
- Palmerini MG, Macchiarelli G, Cocciolone D, Mascitti IA, Placidi M, Vergara T, Di Emidio G, Tatone C. 2023. Modulating morphological and redox/glycative alterations in the pcos uterus: effects of carnitines in pcos mice. Biomedicines 11:374. DOI: 10.3390/biomedicines11020374.
- Ren J, Tan G, Ren X, Lu W, Peng Q, Tang J, Wang Y, Xie B, Wang M. 2022. The PNA mouse may be the best animal model of polycystic ovary syndrome. Frontiers in Endocrinology 13: 950105. DOI: 10.3389/fendo.2022.950105
- Sander V, Luchetti CG, Solano ME, Elia E, Di Girolamo G, Gonzalez C, Motta AB. 2006. Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone. Reproduction 131: 591–602. DOI: 10.1530/rep.1.00941
- Shi D, Vine DF. 2009. Animal models of polycystic ovary syndrome : a focused review of rodent models in relationship to clinical phenotypes and cardiometabolic risk. Fertility and Sterility 98:185-193.e2. DOI: 10.1016/j.fertnstert.2012.04.006
- Tsui KH, Lin L Te, Chang R, Huang BS, Cheng JT, Wang PH. 2015. Effects of dehydroepiandrosterone supplementation on women with poor ovarian response: A preliminary report and review. Taiwanese Journal of Obstetrics & Gynecology 54: 131–136. DOI: T10.1016/j.tjog.2014.07.007
- Walters KA, Allan CM, Handelsman DJ. 2012. Rodent models for human polycystic ovary syndrome. Biology of Reproduction 86: 1–12. DOI: 10.1095/biolreprod.111.097808
- Wang X, Gu L, Zhang Y, Xiong C, Peng Y, Ding X. 2022. Effects of dehydroepiandrosterone alone or in combination with a high-fat diet and antibiotic cocktail on the heterogeneous phenotypes of PCOS mouse models by regulating gut microbiota. Frontiers in Endocrinology 13:1–13. DOI: 10.3389/fendo.2022.1030151
- Wu H, Zhao B, Yao Q, Kang J. 2023. Dehydroepiandrosterone‑induced polycystic ovary syndrome mouse model requires continous treatments to maintain reproductive phenotypes. Journal of Ovarian Research 16: 207. DOI: 10.1186/s13048-023-01299-8
- Zhang R, Hu K, Bai H, Liu H, Pu Y, Yang C, Liu Q, Fan P. 2024. Increased oxidative stress is associated with hyperandrogenemia in polycystic ovary syndrome evidenced by oxidized lipoproteins stimulating rat ovarian androgen synthesis in vitro. Endocrine 19 Feb: 1-12. DOI: 10.1007/s12020-024-03726-2
- Zhao Y, Wang J, Qin W, Hu Q, Li J, Qin R, Ma N, Zheng F, Tian W, Jiang J, Huang J, Qin A. 2024. DHEA promotes ovarian angiogenesis and improves ovarian function in POI rats by up-regulating HIF-1α/VEGF signalling. Reproductive Biomedicine Online 0:103914. DOI: 10.1016/j.rbmo.2024.103914
References
Azziz R. 2006. Diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature. Journal of Clinical Endocrinology and Metabolism. 91:781–785. DOI: 10.1210/jc.2005-2153
Deswal R, Narwal V, Dang A, Pundir CS. 2020. The prevalence of polycystic ovary syndrome: a brief systematic review. Journal of Human Reproductive Science 13: 261–271. DOI: 10.4103/jhrs.JHRS_95_18
Fahed G, Aoun L, Zerdan MB, Allam S, Zerdan MB, Bouferraa Y, Assi HI. 2022. Metabolic syndrome: updates on pathophysiology and management in 2021. International Journal of Molecular Sciences 23: 786. DOI: 10.3390/ijms23020786
Fu L, Xie N, Qu F, Zhou J, Wang F. 2023. The association between polycystic ovary syndrome and metabolic syndrome in adolescents: a systematic review and meta-analysis. Reproductive Sciences 30: 28. DOI: 10.1007/s43032-022-00864-8
Karee M, Gundabattula SR, Sashi L, Boorugu H. 2020. Prevalence of metabolic syndrome in women with polycystic ovary syndrome and the factors associated : A cross sectional study at a tertiary care center in Hyderabad, south-eastern India. Diabetes and Metabolic Syndrom 14:583–587. DOI: 10.1016/j.dsx.2020.05.006
Li Y, Zheng Q, Sun D, Cui X, Chen S, Bulbul A, Liu S, Yan Q. 2019. Dehydroepiandrosterone stimulates inflammation and impairs ovarian functions of polycystic ovary syndrome. Journal of Cellular Physiology 234: 7435–7447. DOI: 10.1002/jcp.27501
Lorincz CE, Börzsei D, Hoffmann A, Varga C, Szabó R. 2024. Mechanisms and target parameters in relation to polycystic ovary syndrome and physical exercise : focus on the master triad of hormonal changes, oxidative stress, and inflammation. Biomedicines 12: 560. DOI: 10.3390/biomedicines12030560
Osuka S, Nakanishi N, Murase T, Nakamura T, Goto M, Iwase A, Kikkawa F. 2018. Animal models of polycystic ovary syndrome: A review of hormone‐induced rodent models focused on hypothalamus‐pituitary‐ovary axis and neuropeptides. Reproductive Medicine and Biology 18: 151–160. DOI: 10.1002/rmb2.12262
Palmerini MG, Macchiarelli G, Cocciolone D, Mascitti IA, Placidi M, Vergara T, Di Emidio G, Tatone C. 2023. Modulating morphological and redox/glycative alterations in the pcos uterus: effects of carnitines in pcos mice. Biomedicines 11:374. DOI: 10.3390/biomedicines11020374.
Ren J, Tan G, Ren X, Lu W, Peng Q, Tang J, Wang Y, Xie B, Wang M. 2022. The PNA mouse may be the best animal model of polycystic ovary syndrome. Frontiers in Endocrinology 13: 950105. DOI: 10.3389/fendo.2022.950105
Sander V, Luchetti CG, Solano ME, Elia E, Di Girolamo G, Gonzalez C, Motta AB. 2006. Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone. Reproduction 131: 591–602. DOI: 10.1530/rep.1.00941
Shi D, Vine DF. 2009. Animal models of polycystic ovary syndrome : a focused review of rodent models in relationship to clinical phenotypes and cardiometabolic risk. Fertility and Sterility 98:185-193.e2. DOI: 10.1016/j.fertnstert.2012.04.006
Tsui KH, Lin L Te, Chang R, Huang BS, Cheng JT, Wang PH. 2015. Effects of dehydroepiandrosterone supplementation on women with poor ovarian response: A preliminary report and review. Taiwanese Journal of Obstetrics & Gynecology 54: 131–136. DOI: T10.1016/j.tjog.2014.07.007
Walters KA, Allan CM, Handelsman DJ. 2012. Rodent models for human polycystic ovary syndrome. Biology of Reproduction 86: 1–12. DOI: 10.1095/biolreprod.111.097808
Wang X, Gu L, Zhang Y, Xiong C, Peng Y, Ding X. 2022. Effects of dehydroepiandrosterone alone or in combination with a high-fat diet and antibiotic cocktail on the heterogeneous phenotypes of PCOS mouse models by regulating gut microbiota. Frontiers in Endocrinology 13:1–13. DOI: 10.3389/fendo.2022.1030151
Wu H, Zhao B, Yao Q, Kang J. 2023. Dehydroepiandrosterone‑induced polycystic ovary syndrome mouse model requires continous treatments to maintain reproductive phenotypes. Journal of Ovarian Research 16: 207. DOI: 10.1186/s13048-023-01299-8
Zhang R, Hu K, Bai H, Liu H, Pu Y, Yang C, Liu Q, Fan P. 2024. Increased oxidative stress is associated with hyperandrogenemia in polycystic ovary syndrome evidenced by oxidized lipoproteins stimulating rat ovarian androgen synthesis in vitro. Endocrine 19 Feb: 1-12. DOI: 10.1007/s12020-024-03726-2
Zhao Y, Wang J, Qin W, Hu Q, Li J, Qin R, Ma N, Zheng F, Tian W, Jiang J, Huang J, Qin A. 2024. DHEA promotes ovarian angiogenesis and improves ovarian function in POI rats by up-regulating HIF-1α/VEGF signalling. Reproductive Biomedicine Online 0:103914. DOI: 10.1016/j.rbmo.2024.103914