ArticleAmerican journal of physiology. Endocrinology and metabolism2026
Testosterone deficiency synergistically exacerbates fructose-induced hepatic steatosis through gut microbiota and pyruvate in mice.
Article in American journal of physiology. Endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Estradiol mitigates lipid accumulation, oxidative stress, apoptosis, and MAPKs activation in NASH rat model with bilateral orchidectomy.PNAS nexus · 2026Article
- Sugar Shockwaves: How the Fructose-Glucose-ChREBP Pathway Hijacks Liver Metabolism.Life (Basel, Switzerland) · 2026Review
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11 authors.
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Abstract
Hepatic steatosis is the initial stage of metabolic dysfunction-associated steatotic liver disease (MASLD) and is highly prevalent among middle-aged men. Low testosterone levels and dietary fructose intake are independent risk factors for MASLD, although these can occur simultaneously. This study investigated the combined effects of testosterone deficiency and fructose intake on hepatic steatosis, focusing on the involvement of gut microbiota. Male mice were castrated or sham-operated at 8 wk of age and administered fructose water with or without antibiotics for 8 wk after being divided into six groups: Sham/Control, Sham/Fructose, Sham/Fructose + Antibiotics, Castration/Control, Castration/Fructose, and Castration/Fructose + Antibiotics. The castrated groups had lower body weights than the sham-operated groups, whereas castration did not affect portal and circulating fructose concentrations. Although castration alone did not affect hepatic lipid accumulation, it synergistically promoted fructose-induced triglyceride accumulation, which was alleviated by antibiotic treatment. The expression of lipogenesis-related genes (
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