We
explored the effects of dietary supplementation with phlorizin
on redox state-related gut microbiota homeostasis in an obesity mouse
model. Mice (C57BL/6J) were grouped as follows for 12 weeks: normal
chow diet group (NCD), high-fat and cholesterol diet group (HFD),
and treatment groups fed with HFD along with three levels of phlorizin.
Phlorizin alleviated the hyperlipidemia and redox status and increased
the total ccal SCFA content (1.88 ± 0.25 mg/g). Additionally,
phlorizin regulated gene expression related to lipid metabolism, redox
status, and cecum barrier and rebuilt gut microbiota homeostasis.
After interference by antibiotics, the total phloretin content in
the feces was decreased about 4-fold, and most of the health-promoting
effects were abolished, indicating that phlorizin might be susceptible
to microbial biotransformation and that microecology is indispensable
for maintaining the redox state capacities of phlorizin. Phlorizin
treatment could be an advantageous option for improving HFD-related
obesity and redox states related to gut microbiota homeostasis.
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