Fructooligosaccharide supplementation ameliorates gut associated metabolic dysregulation in estrogen-deprived rats via targeting oxidative stress, inflammation, apoptosis, and gut microbiome.
AI Summary
Key Findings
Abstract
Estrogen is a key regulatory hormone that maintains metabolic and gut homeostasis by modulating immune responses, microbial composition, and energy balance. However, estrogen deficiency is strongly associated with gut associated metabolic dysregulation (GAMD), characterised by increased oxidative stress, systemic inflammation, and altered gut microbiome (GM). Prebiotic compounds such as fructooligosaccharide (FOS) have shown potential in modulating gut and metabolic health. This study aimed to assess the therapeutic potential of FOS supplementation in restoring GAMD in estrogen-deprived rats. To induce GAMD, female Sprague-Dawley rats were bilaterally ovariectomized (OVX) and fed FOS for 28 days to restore the gut and associated metabolic functions. At the end, various physiological, anthropometric, and adiposity markers were assessed. Further, oxidative stress, inflammation, apoptosis, and histopathological parameters were evaluated in the colon and liver. Furthermore, gut mucosa, tight junction gene (TJG), and GM were also analysed. OVX rats fed FOS (50&100 mg/kg) for 28 days showed recovery of basic physiological, anthropometric, and adiposity markers. There was also a substantial reduction in apoptosis, inflammation, and oxidative stress in both the colon&liver. Additionally, gut mucosa, TJG, and GM were restored. Histopathological examinations revealed improved gut integrity (mucosal layer&goblet cells) and liver health (healthy hepatocytes). FOS ameliorates the postmenopausal GAMD by targeting oxidative stress, inflammation, and GM. Therefore, FOS may be a promising candidate for preventing postmenopausal complications in clinical settings.
Affiliation
Seema Bansal
External References
- PubMed ID:
- 42236502
Comments
Sign in or create a free account to join the conversation.
Sign in to commentBe the first to comment.