Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

OR15-3 Contribution of Hyperandrogenemia to Dysbiosis, Gut Inflammation, and Dysregulation of Short-Chain Fatty Acid Homeostasis in Mouse Model of Polycystic Ovary Syndrome

Animal Study with a reported sample of 8, published in J Endocr Soc (2022) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
J Endocr Soc (2022)
Reported sample size
8
Source database
Europe PMC
PMCID
PMC9625776

Abstract (original English)

Abstract Introduction and Purpose Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Notably, PCOS women with hyperandrogenism have a pronounced increased risk for cardio-metabolic comorbidities. The gut microbiome is responsible for fermentation of indigestible fiber to produce short-chain fatty acids (SCFA), which help maintain metabolic function and reduce gut inflammation. Alteration in the gut microbiome, or dysbiosis, affects overall metabolic homeostasis and contributes to pathogenesis of metabolic diseases. While dysbiosis has been observed in women with PCOS, the molecular mechanisms of hyperandrogenemia-induced dysbiosis and its contribution to SCFA excretion and gut inflammation have not been studied in PCOS. Methods Four-week old C57BL/6N female mice were implanted subcutaneously with dihydrotestosterone (DHT, 8.0 mg) or vehicle silastic tubes (n=8/grp). Animals were treated day 90 and the gastrointestinal tract was collected. Expression levels of mRNA were assessed by RT-qPCR. Fecal microbiota was assessed by 16S rRNA gene sequencing and profiled using MicrobiomeAnalyst; SCFA concentrations were assessed by LC-MS. Results DHT-treated female mice had significantly increased lean mass (21.35 ± 0.84 vs 19.25 ± 0.55 g, p Conclusions Androgen-mediated gut dysbiosis may contribute to altered glucose handling, adiposity, a

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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