Dr. Umar

This study explored gut microbiota in DHT-induced PCOS rats and showed that Diane-35 and probiotics restored microbial diversity, while berberine reduced it. Key microbial signatures linked directly to metabolic and reproductive

The study identifies distinct microbial and functional dysbiosis in the IR-PCOS gut microbiome, marked by elevated Bacteroidaceae, reduced Prevotellaceae, and inflammation-linked pathways that may worsen hormonal and metabolic dysfunction.

This study links altered gut microbiota with distinct fecal lipid metabolites and androgen levels in obese PCOS, identifying diagnostic microbial and metabolic signatures that help explain hormonal and metabolic dysfunction.

Shotgun metagenomics revealed distinct PCOS gut microbiome signatures linked to inflammation, elevated reproductive hormones, and metabolic dysfunction, highlighting mechanistic roles for pathogenic species and potential for microbiome-directed therapies.

Androgen-induced gut dysbiosis in PCOS worsens metabolic and endocrine dysfunction. FMT experiments show dysbiotic microbiota can independently trigger hyperandrogenism, glucose intolerance, and ovarian abnormalities through gut–liver and gut–brain pathways.

Normal-weight women with insulin-resistant PCOS show distinct gut microbiome signatures, particularly increased Enterococcus and Rothia and reduced Prevotella, linking microbial shifts to metabolic dysfunction and insulin resistance.

Multi-omics profiling revealed a distinct PCOS microbiome signature linking inflammatory taxa, disrupted lipid metabolites, and hormonal dysregulation. Integrating seven microbial species with three metabolites achieved perfect diagnostic accuracy, supporting a causal gut–metabolism axis.

This study identifies distinct gut-microbiome and SCFA alterations in PCOS, linking specific taxa and fatty acids with hyperandrogenism, inflammation, and gut permeability.

Diet shaped gut microbiota more strongly than PCOS pathology, yet PCOS selectively reduced beneficial Bacteroides acidifaciens. FMT shifted microbial profiles toward normal but did not reverse metabolic or reproductive traits, highlighting diet-microbe interactions as potential therapeutic levers.

Orlistat treatment reshaped gut microbiota and fecal metabolites in a PCOS rat model, lowering androgenic metabolites and shifting microbial taxa toward anti-inflammatory profiles that align with improved metabolic and hormonal balance.

This study shows how L. reuteri protects against circadian disruption–induced PCOS dyslipidemia by lowering capric acid and inhibiting hepatic GALR1 signaling, driven by microbiome restructuring.

This study links reduced butyric acid in PCOS to increased METTL3-mediated m6A methylation and ovarian inflammation, showing that butyrate supplementation corrects microbial, epigenetic, and inflammatory imbalances in granulosa cells and PCOS mice.

WEA improved PCOS in rats by restoring ovarian signaling pathways and remodeling gut microbiota, increasing taxa such as Bifidobacterium animalis and Lactobacillus murinus. These findings highlight microbiome-mediated mechanisms linking botanical therapy to metabolic and reproductive improvements.

Omega-3 PUFAs gut microbiota PCOS interactions were tested in DHEA-induced mice, revealing both microbial and direct ovarian anti-inflammatory effects that improved metabolic and reproductive dysfunction.

The study shows that a ketogenic diet reshapes the gut microbiome and reduces steroidogenic metabolites in a PCOS rat model, linking microbial changes to improved insulin resistance and androgen excess.

Quinoa improved hormonal, metabolic, ovarian, and gut microbial disturbances in a PCOS rat model by restoring PI3K/AKT/mTOR signaling, reducing excess autophagy, and correcting dysbiosis.

Inulin supplementation in obese PCOS patients improved gut microbiota balance, reduced inflammation, and shifted sex hormone and metabolic markers toward healthier profiles, supporting microbiome-targeted therapy as a promising adjunct in PCOS management.

This study details dysbiotic alteration in the fecal microbiota of patients with PCOS, showing reduced diversity, disrupted SCFA-producing genera, and distinct functional microbial changes linked to metabolic dysfunction.

Metformin altered plasma microbial EVs in PCOS-IR, increasing diversity and elevating Streptococcus salivarius EVs, suggesting microbiome-mediated metabolic benefits.

Irisin improved reproductive and microbiome-metabolome disturbances in PCOS mice, reversing hyperandrogenism, restoring folliculogenesis, and shifting key bacterial and metabolic signatures toward a healthier profile.

A high-fat, high-fructose diet exerted stronger effects on gut microbiota than letrozole-induced PCOS in prepubertal mice, reducing SCFAs, increasing LPS, and altering key genera linked to lipid metabolism and PCOS-related metabolic disruption.

Irisin improved reproductive and microbial abnormalities in PCOS mice, reversing key gut taxa shifts and metabolite elevations while restoring ovarian function. Findings suggest an irisin–microbiota axis relevant for PCOS therapies.

BL21 improved metabolic, hormonal, inflammatory, and microbiome dysfunction in a DHT-induced PCOS model, restoring beneficial taxa and supporting gut–brain–ovary axis regulation.

This study compared gut microbiota in Japanese women with and without PMS, identifying higher diversity and increased Collinsella, Bifidobacterium, and Blautia in PMS, suggesting microbial signatures relevant to symptom development.