Recent studies demonstrate that SCFAs affect bone metabolism via the processes outlined ( Figure 2 ): Intestinal Epithelial Function and Mineral Absorption: SCFAs act on IECs to promote their development and differentiation, hence affecting the mechanical, chemical, immune, and biological barriers of the intestinal mucosa, regulating electrolyte exchange (such as between mineral ions and hydrogen ions), lowering luminal pH, and directly improving the absorption of minerals specially calcium (99, 100);Systemic Signaling via G protein-coupled receptors (GPCRs): Upon entering systemic circulation, SCFAs interact with GPCRs, influencing metabolism and function in peripheral tissues, including adipose tissue, skeletal muscle, bone, and liver (101);Epigenetic Regulation: SCFAs block histone deacetylases (HDACs), therefore contributing to the epigenetic regulation of gene expression, which may influence bone metabolism (102, 103);Modulation of Inflammatory Cytokines: SCFAs can modulate the production of inflammatory factors, therefore affecting bone remodeling (104)
In contrast, inhibition of SCD1/FADS2 directly downregulated the expression of GPX4 and reduced the ratio of GSH/GSSG, thereby accelerating iron-mediated lipid peroxidation, mitochondrial dysfunction and ferroptosis[117]
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15 Being a powerful antioxidant, glutathione plays a critical role in several metabolic pathways: DNA and protein synthesis, amino acid transport, enzyme activation, immune system function, scavenging free radicals eg hydrogen peroxide, cofactor in Phase I cytochrome P450 enzyme-mediated detoxification, amino acid translocation across cell membranes, detoxification of xenobiotics, maintenance of sulfhydryl groups of proteins, mitochondrial function and maintenance of mitochondrial DNA, catalysis of exchange reactions and many more
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C., Quiceno, D
