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https://www.tandfonline.com/doi/abs/10.1080/09513590.2019.1576616?journalCode=igye20

https://www.ncbi.nlm.nih.gov/pubmed/30806529?dopt=Abstract [Read more…] about Potential roles of carnitine in patients with polycystic ovary syndrome: a systematic review

https://link.springer.com/article/10.1007%2Fs11154-019-09482-3

https://www.ncbi.nlm.nih.gov/pubmed/30798426?dopt=Abstract

Differential activity of the corticosteroidogenic enzymes in normal cycling women and women with polycystic ovary syndrome.

Rev Endocr Metab Disord. 2019 Feb 23;:

Authors: Yamamoto MMW, de Medeiros SF

Abstract

The phenotypic complex of patients with definitive diagnosis of polycystic ovary syndrome may include patients with normal and high serum androgen levels. Patients with hyperandrogenemia seem to present higher risk of changes to the glucose and lipid metabolism and, eventually, of earlier development of cardiovascular diseases than normoandrogenemic patients or healthy women. From a laboratory and clinical point of view, it is important to check androgen levels in patients with polycystic ovary syndrome. The identification of partial insufficiency of a given corticosteroidogenic enzyme is also relevant to understand the physiopathology of androgen increase in polycystic ovary syndrome. Therefore, the present review analyzes the functions of the different enzymes involved in the ovary and adrenal steroidogenesis in normal cycling women and in patients with polycystic ovary syndrome. In addition, it emphasizes appropriate reason for investigating eventual enzyme deficiency to provide rationale for prescription and follow-up of women with polycystic ovary syndrome.

PMID: 30798426 [PubMed – as supplied by publisher]

AMH signaling cascade plays an important role in PCOS etiology.

https://academic.oup.com/jcem/advance-article-abstract/doi/10.1210/jc.2018-02178/5342940?redirectedFrom=fulltext

https://www.ncbi.nlm.nih.gov/pubmed/30786001?dopt=Abstract

Functional Genetic Variation in the Anti-Müllerian Hormone Pathway in Women with Polycystic Ovary Syndrome.

J Clin Endocrinol Metab. 2019 Feb 20;:

Authors: Gorsic LK, Dapas M, Legro RS, Hayes MG, Urbanek M

Abstract

CONTEXT: PCOS is a highly heritable, common endocrine disorder characterized by hyperandrogenism, irregular menses and polycystic ovaries. PCOS is often accompanied by elevated levels of anti-Müllerian hormone (AMH). AMH inhibits follicle maturation. AMH also inhibits steroidogenesis through transcriptional repression of CYP17A1. We recently identified 16 rare PCOS-specific pathogenic variants in AMH.

OBJECTIVE: To test whether additional members of the AMH signaling pathway also contribute to the etiology of PCOS.

PARTICIPANTS/METHODS: Targeted re-sequencing of coding and regulatory regions of AMH and its specific type 2 receptor, AMHR2 was performed on 608 PCOS-affected women and 142 reproductively normal control women. Prediction tools of deleteriousness and in silico evidence of epigenetic modification were used to prioritize variants for functional evaluation. Dual luciferase reporter assays and splicing assays were used to measure the impact of genetic variants on function.

RESULTS: We identified 20 additional variants in/near AMH and AMHR2 with significantly reduced signaling activity in in vitro assays. Collectively, from our previous study and reported herein, we have identified a total of 37 variants with impaired activity in/near AMH and AMHR2 in 41 women affected with PCOS, or 6.7% of our PCOS cohort. Furthermore, no functional variants were observed in the 142 phenotyped controls. The functional variants were significantly associated with PCOS in our cohort of 608 women with PCOS and 142 controls (p=2.3 x 10-5) and very strongly associated with PCOS relative to a larger non-Finnish European (gnomAD) population-based control cohort (p<1×10-9).

CONCLUSIONS: AMH signaling cascade plays an important role in PCOS etiology.

PMID: 30786001 [PubMed – as supplied by publisher]

https://www.ncbi.nlm.nih.gov/pubmed/30672430?dopt=Abstract

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Patatin-like phospholipase domain containing 3-gene (adiponutrin), preptin, kisspeptin and amylin regulates oocyte developmental capacity in PCOS.

Cell Mol Biol (Noisy-le-grand). 2018 Dec 31;64(15):7-12

Authors: Celik N, Aydin S, Ugur K, Yardim M, Acet M, Yavuzkir S, Sahin İ, Celik O

Abstract

This study was planned to test whether follicular fluid (FF) levels of patatin-like phospholipase domain containing 3-gene (PNPLA3:adiponutrin), preptin, kisspeptin, and amylin change in polycystic ovarian syndrome (PCOS). A total of 40 infertile volunteers undergoing IVF/ICSI were included in the study. They were divided into two groups as PCOS (n=20) and control group without PCOS (n=20). The controls were recruited from subjects with a poor ovarian response. The PCOS and control participants were matched according to their body mass index (BMI). Each group of participants underwent ovarian stimulation with GnRH antagonist protocol. Blood and FF samples of one dominant follicle were obtained from each subject during the oocyte pick-up. FF and serum levels of PNPLA3, preptin, kisspeptin and amylin were measured through ELISA. Amylin and adiponutrin median values were not different according to study groups (p>0.05). FF-preptin median values in the control group were similar to the serum preptin values of control and PCOS groups (Z=0.970, p=1.000 and Z=2.631, p=0.051, respectively). Medians of the serum preptin in control and PCOS groups were the same (Z=1.649; p=0.595). FF-preptin median values of PCOS group were significantly lower than the preptin median values of the control group. Serum preptin levels were positively correlated with HOMA-IR, but not with pregnancy rates and the number of retrieved oocytes. Serum kisspeptin levels were negatively correlated with the number of retrieved oocytes and pregnancy rates. While amylin and adiponutrin have no role in the folliculogenesis, kisspeptin and preptin work together for regulating follicle developmental capacity in PCOS.

PMID: 30672430 [PubMed – indexed for MEDLINE]

Abnormal expression of PPARγ mRNA in ovarian granulosa cells may be related to the mechanism of PCOS.

https://www.ncbi.nlm.nih.gov/pubmed/30783446?dopt=Abstract

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Effect of testosterone on the expression of PPARγ mRNA in PCOS patients.

Exp Ther Med. 2019 Mar;17(3):1761-1765

Authors: Cao J, Maowulieti G, Yu T

Abstract

Expression of peroxisome proliferator-activated receptor γ (PPARγ) mRNA in ovarian granulosa cells of patients with polycystic ovary syndrome (PCOS) were explored. Ovarian granulosa cells were extracted from 5 patients with PCOS and 30 normal controls. Expression of PPARγ mRNA in granulosa cells of the 5 PCOS patients (observation group) and 5 normal controls (control group) was detected by RT-qPCR. The remaining 25 cases of normal human ovarian granulosa cells were cultured in vitro for 48 h, followed by cell culture for another 24 h with different concentrations of testosterone, insulin (INS), and rosiglitazone (RGZ). After that, expression of PPARγ mRNA was detected by RT-qPCR. Relative expression level of PPARγ mRNA in the observation group was significantly lower than that in the control group. Compared with testosterone concentration at 10-2 mol/ml, testosterone concentration at 10-3 mol/ml significantly reduced the expression level of PPARγ mRNA. When the INS concentration was 10-5 mol/ml, relative expression level of PPARγ mRNA was significantly higher than that of the control group (P<0.01). Relative expression level of PPARγ mRNA was significantly higher than that of the control group when INS concentration was 10-4 mol/ml. When the concentration of RGZ was 10-4 mol/ml, the relative expression level of PPARγ mRNA was significantly higher than that of the control group (P<0.01). When concentration of RGZ was 10-3 mol/ml, expression level of PPARγ mRNA was significantly increased comparing to that under a RGZ concentration of 10-4 mol/ml or that of the control group (P<0.01). Appropriate concentrations of testosterone can inhibit the expression of PPARγ mRNA in ovarian granulosa cells, and certain concentrations of INS and RGZ can induce the expression of PPARγ mRNA in ovarian granulosa cells. Abnormal expression of PPARγ mRNA in ovarian granulosa cells may be related to the mechanism of PCOS.

PMID: 30783446 [PubMed]

https://www.sciencedirect.com/science/article/pii/S2225411018300154?via%3Dihub

https://www.ncbi.nlm.nih.gov/pubmed/31453130?dopt=Abstract

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Effect of Vitex negundo L. seeds in letrozole induced polycystic ovarian syndrome.

J Tradit Complement Med. 2019 Oct;9(4):336-345

Authors: Kakadia N, Patel P, Deshpande S, Shah G

Abstract

The clinical management of PCOS is multifaceted but often unsatisfactory. The aim of the current study is to evaluate the effect of Vitex negundo L. in the letrozole-induced polycystic ovarian syndrome. Female Sprague-Dawley rats were divided into six groups, each containing 6 animals. Group I (Control) daily received 1% carboxymethylcellulose (CMC) suspension as a vehicle control. Letrozole (1 mg/kg) was administered per orally (p.o) for a period of 21 days for the induction of PCOS in Group II to VI. PCOS induced animals were treated with aqueous (Group III – 200 mg/kg and IV- 400 mg/kg) and hydroalcoholic extract (Group V- 200 mg/kg and VI- 400 mg/kg) of Vitex negundo up to 66 days using 0.5% w/v CMC as the vehicle. Body weight and estrous cycle phase were measured every day. Blood samples were collected on 0, 21 and 66 days for the measurement of fasting blood glucose, lipid profile, LH, FSH and hormonal level. Oral glucose tolerance test was performed to study insulin resistance effect. Toxicity markers; SGOT, SGPT, and creatinine also measured at the end of the study. The administration of Letrozole led to an abnormality in serum sex steroid profile, lipid profile, glucose and estrous cycle. It was able to successfully exert its protective effect by restoring parameters to the normal level and disappearance of cysts in ovaries. This can be attributed to phyto-components present in the extract. The aqueous and hydro-alcoholic extracts of seeds of Vitex negundo showed significant amelioration of Letrozole induced PCOS.

PMID: 31453130 [PubMed]