Gut Microbiota Has the Potential to Improve Sarcopenic Obesity in Menopausal Women by Regulating Estrogen

Sarcopenic obesity (SO) in menopausal women, characterized by concurrent skeletal muscle loss and visceral adiposity, is primarily driven by estrogen deficiency. Emerging evidence suggests that the gut microbiota, through its "estrobolome" function, may significantly influence SO pathogenesis by modulating estrogen metabolism and muscle-adipose crosstalk.

To systematically review the mechanisms linking the gut microbiota, estrogen metabolism, and SO risk in menopausal women.

We synthesized findings from animal models, mechanistic studies, and small-scale human trials investigating the microbiota-estrogen-muscle/adipose axis.

Menopause reduced the abundance of the gut microbial β-glucuronidase, impairing enterohepatic estrogen recirculation. Dysbiosis activates the LPS-TLR4 pathway, promoting muscle catabolism via MuRF1 up-regulation and adipose inflammation. Short-chain fatty acids enhance insulin sensitivity through GLP-1 stimulation. Population studies have demonstrated reduced microbiota diversity and altered Firmicutes/Bacteroidetes ratios in postmenopausal women, which correlates with systemic inflammation and metabolic dysfunction. Intervention studies using combined soy isoflavones and probiotics have shown lipid benefits, but muscle effects remain unevaluated.

The gut microbiota-estrogen axis is a promising therapeutic target for menopausal SO; however, current evidence is limited to preclinical models and small human trials. Rigorous large-scale randomized controlled trials are essential to establish efficacy and safety before microbiota-based interventions can be recommended as adjunctive therapies.