The antidiabetic effects of Fu brick
tea aqueous extract (FTE)
and its underlying molecular mechanism in type 2 diabetes mellitus
(T2DM) mice were investigated. FTE treatment significantly relieved
dyslipidemia, insulin resistance (IR), and hepatic oxidative stress
caused by T2DM. FTE also ameliorated the T2DM-induced gut dysbiosis
by decreasing the Firmicutes/Bacteroidota (F/B) ratio at the phylum level and
promoting the proliferation of Bifidobacterium, Parabacteroides, and Roseburia at the genus level. Besides, FTE significantly
improved colonic short-chain fatty acid levels of T2DM mice. Furthermore,
the antidiabetic effects of FTE were proved to be mediated by the
IRS1/PI3K/Akt and AMPK-mediated gluconeogenesis signaling pathways.
Metabolomics analysis illustrated that FTE recovered the levels of
28 metabolites associated with T2DM to the levels of normal mice.
Taken together, these findings suggest that FTE can alleviate T2DM
by reshaping the gut microbiota, activating the IRS1/PI3K/Akt pathway,
and regulating intestinal metabolites.
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