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.
Monitoring chemical contamination in water is a must to guarantee the supply to the society of this more and more scarce prized asset. The European Union as well as other bodies have released reports and directives defining lists of substances whose detection in waters should be prioritized and posing limits to the maximum allowable concentrations that drinking water must have. The scientific community has been actively working on the development of analytical tools that could be applied in the detection of hazardous chemical species in waters. Here, an overview of electrochemical devices with the potential of being implemented to the monitoring of the forty five pollutants include in the list of priority substances set in the 2013 EU directive that could be grouped into heavy metals, pesticides, hydrocarbons, halogenated hydrocarbons and alkyl phenols, is given, aiming at showing their benefits and limitations in this scenario.
This study was designed to first verify the protective
capacity
of turmeric powder (TP) as a traditional cooking spice against dextran
sulfate sodium (DSS)-induced intestinal inflammation and intestine
microbiota imbalance. The DSS-induced mice were fed a standard rodent
chow supplemented with or without TP (8%) for 37 days. The results
indicated that the pathological phenotype, gut barrier disruption,
and colon inflammation of DSS-induced mice were significantly improved
through supplementation of TP. In addition, 16S rRNA-based microbiota
or targeted metabolomics analysis indicated that TP ameliorated intestinal
microbiota dysbiosis caused by DSS and particularly enhanced the abundances
of probiotics correlated with tryptophan metabolism, such as Lactobacillus and Bifidobacterium, where the cecal tryptophan was metabolized to indole-3-propionic
acid and indole-3-acetic acid. Consumption of TP markedly enhanced
the expression levels of colonic aromatic hydrocarbon receptors and
further increased the expressions of intestinal tight junction proteins
and interleukin-22 in the colitis mice. Collectively, these findings
manifest the protective actions of dietary TP consumption against
ulcerative colitis via restoring the intestinal microbiota disorders,
promoting microbial metabolism, and improving intestinal barrier damage.
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