Correlation between glucose metabolism and serum steroid hormones in patients with polycystic ovary syndrome

Li, Xuelin; Zhang, Tianyue; Li, Shengxian; Deng, Yuying; Wang, Lihua; Tao, Tao; Wang, Shujie; Gu, Yuchao; Gu, Weiqiong; Hong, Jie; Liu, Wei; Wang, Weiqing; Zhang, Yifei

doi:10.1111/cen.14154

Cited by 13 publications

(6 citation statements)

References 38 publications

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“…Ovarian follicular development is a highly coordinated and nutrition-sensitive process [ 23 ], and glucose is an important energy substrate for metabolism in the follicles of many species [ 24 , 25 , 26 , 27 ]. Previous studies confirm that short-term dietary supplementation of ewes during the luteal phase can increase fertility due to elevated glucose and steroid hormone concentrations in follicles [ 19 , 28 , 29 ], whereas glucose has deleterious effects on ovary structure and function at higher concentrations [ 5 , 30 , 31 ]. Our previous study also demonstrated that glucose dose had a significant effect on GCs function, with 8.4 mM representing the optimal glucose concentration for GCs to secrete steroid hormones in vitro and a higher concentration of glucose (33.6 mM) inhibiting GCs proliferation and steroidogenesis [ 6 , 7 ].…”

Section: Discussionmentioning

confidence: 99%

LncGSAR Controls Ovarian Granulosa Cell Steroidogenesis via Sponging MiR-125b to Activate SCAP/SREBP Pathway

Wang

Guo²,

Duan³

et al. 2022

IJMS

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Long non-coding RNAs (lncRNAs) have been shown to play important roles in livestock fecundity, and many lncRNAs that affect follicular development and reproductive diseases have been identified in the ovary. However, only a few of them have been functionally annotated and mechanistically validated. In this study, we identified a new lncRNA (lncGSAR) and investigated its effects on the proliferation and steroidogenesis of ovine granulosa cells (GCs). High concentrations of glucose (add 33.6 mM glucose) caused high expression of lncGSAR in GCs by regulating its stability, and lncGSAR overexpression promoted GCs proliferation, estrogen secretion, and inhibited progesterone secretion, whereas interference with lncGASR had the opposite effect. Next, we found that the RNA molecules of lncGSAR act on MiR-125b as competitive endogenous RNA (ceRNA), and SREBP-cleavage-activating protein (SCAP) was verified as a target of MiR-125b. LncGASR overexpression increased the expression of SCAP, SREBP, and steroid hormone-related proteins, which can be attenuated by MiR-125b. Our results demonstrated that lncGSAR can act as a ceRNA to activate SCAP/SREBP signaling by sponging MiR-125b to regulate steroid hormone secretion in GCs. These findings provide new insights into the mechanisms of nutrient-regulated follicle development in ewes.

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Section: Discussionmentioning

confidence: 99%

LncGSAR Controls Ovarian Granulosa Cell Steroidogenesis via Sponging MiR-125b to Activate SCAP/SREBP Pathway

Wang

Guo²,

Duan³

et al. 2022

IJMS

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“…Moreover, Li et al ( 9 ) indicated that propofol inhibited colorectal cancer cell viability and metastasis by regulating the miR-124-3p.1/AKT3 axis. PCOS is a common endocrine disorder with approximate incidence of 10% in women worldwide ( 1 ). The common clinical manifestations of PCOS include hyperandrogenemia, chronic anovulation and sclerocystic ovaries ( 2 , 3 ).…”

Section: Discussionmentioning

confidence: 99%

“…Polycystic ovary syndrome (PCOS) is a universal endocrine disorder, with an incidence of 5-10% in women of childbearing age globally ( 1 , 2 ). The major clinical symptoms in patients with PCOS are subfertility, amenorrhea, seborrhea and acanthosis ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of propofol via the regulation of ovarian granulosa cell proliferation and apoptosis

Ding

Kang

et al. 2021

Exp Ther Med

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Propofol is an anesthetic frequently used in surgery. Accumulating evidence suggests that propofol exhibits an effect on cell viability, apoptosis and invasion in several types of cancer cells. MicroRNAs (miRNAs) have been reported to play pivotal roles in the development of polycystic ovary syndrome (PCOS). However, the diagnostic applications of miR-451a in PCOS remain unknown. The present study aimed to elucidate the effects of propofol on ovarian granulosa cell proliferation and apoptosis and illustrate the specific mechanisms associated with this process. Human ovarian granulosa cell-like KGN cells, which were used as a representative of granulosa cells in the present study, were treated with different concentrations (0, 1, 5 and 10 µg/ml) of propofol for 48 h and cell proliferation and apoptosis were assessed using MTT and flow cytometry assays, respectively. Propofol treatment resulted in significant inhibition of cell viability and induction of apoptosis in KGN cells, which was accompanied with increased cleaved caspase 3 and suppressed pro-caspase 3 expression levels. Furthermore, propofol reduced Wnt3a and β-catenin protein and mRNA expression levels. miR-451a expression in KGN cells was evaluated by reverse transcription-quantitative PCR (RT-qPCR). miR-451a expression was upregulated in propofol-stimulated KGN cells. The data further demonstrated that miR-451a mimics suppressed cell proliferation and increased apoptosis of KGN cells compared with cells transfected with control mimics. Furthermore, the association between miR-451a and propofol was investigated. Rescue experiments were performed to investigate the anti-proliferative mechanism of propofol in ovarian granulosa cells. KGN cells were transfected with miR-451a inhibitor or inhibitor control sequences for 6 h and treated with 10 µg/ml propofol for an additional 48 h. The results from the MTT, RT-qPCR and western blot assays indicated that 10 µg/ml propofol inhibited cell viability, induced apoptosis, enhanced cleaved caspase 3 expression, reduced pro-caspase 3 levels and inhibited the protein and mRNA expression of Wnt3a and β-catenin. However, inhibition of miR-451a demonstrated the opposite effects. In conclusion, the results of the present study revealed that propofol exerted an anti-proliferative and apoptosis-inducing role in ovarian granulosa cells through mediation of miR-451a expression. In addition, the data indicated that miR-451a may be used as an effective therapeutic target for PCOS treatment.

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“…While the exact mechanisms underlying the development of PCOS are not fully understood, genetics and environmental factors are believed to play signi cant roles 12 . Genetic factors may contribute to abnormal insulin signaling, leading to insulin resistance and metabolic disturbances in patients with PCOS 13,14 . Environmental factors, such as an unhealthy diet and lifestyle, may also contribute to PCOS development.…”

Section: Introductionmentioning

confidence: 99%

The role of gut microbiota and inflammatory factors in the pathogenesis of PCOS: A Mendelian Randomization study

Lin,

Wang,

et al. 2024

Preprint

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Background: Polycystic ovary syndrome (PCOS) is a common gynecological disorder, yet its etiology remains incompletely understood. Recent studies have suggested that gut microbiota dysbiosis and inflammation could potentially contribute to the development of PCOS. Methods: In this study, we employed Mendelian randomization (MR) analysis to investigate the relationship between gut microbiota, inflammatory factors, and PCOS development. Publicly available genome-wide association study (GWAS) data were utilized, and MR analysis was conducted to assess the causal relationships between them. Results: The study revealed potential causal relationships between certain taxonomic groups within the gut microbiota and the risk of PCOS development. Specifically, taxa such as the phylum Cyanobacteria, the order Burkholderiales, the genus Holdemania, the genus Candidatus Soleaferrea, the genus Blautia, and the genus Bilophila exhibited negative associations with the risk of PCOS, suggesting a protective effect against the condition. Conversely, taxa such as the family Lachnospiraceae, the class Bacilli, and the class Alphaproteobacteria showed positive associations with the risk of PCOS, potentially increasing susceptibility to the disease. Additionally, the study identified inflammatory factors such as CCL2, IL-12, and IL18Ra as having potential causal relationships with the risk of PCOS. Conclusion: The findings of this study indicate that both gut microbiota and inflammatory factors may play significant roles in the pathogenesis of PCOS. Gut microbiota dysbiosis may contribute to exacerbated inflammatory responses, potentially influencing the development of PCOS. Further research endeavors can delve deeper into elucidating the specific roles and interactions between gut microbiota and inflammatory factors in the pathogenesis of PCOS. This could open up novel avenues for the diagnosis and treatment of PCOS by identifying new targets and therapeutic strategies.

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Correlation between glucose metabolism and serum steroid hormones in patients with polycystic ovary syndrome

Cited by 13 publications

References 38 publications

LncGSAR Controls Ovarian Granulosa Cell Steroidogenesis via Sponging MiR-125b to Activate SCAP/SREBP Pathway

LncGSAR Controls Ovarian Granulosa Cell Steroidogenesis via Sponging MiR-125b to Activate SCAP/SREBP Pathway

Protective effect of propofol via the regulation of ovarian granulosa cell proliferation and apoptosis

The role of gut microbiota and inflammatory factors in the pathogenesis of PCOS: A Mendelian Randomization study

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