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Potential direct anti-inflammatory mechanisms from preclinical and early clinical studies include: Modulation of immune cell function : GLP-1 receptor activation may reduce pro-inflammatory cytokine production from macrophages and other immune cells Reduction of oxidative stress : These medications may decrease reactive oxygen species production, which contributes to inflammatory processes Endothelial protection : GLP-1 receptor agonists may improve endothelial function and reduce vascular inflammation Inhibition of inflammatory signalling pathways : Including suppression of nuclear factor-kappa B (NF-B), a key regulator of inflammatory gene expression It's important to note that many of these mechanisms have been primarily demonstrated in laboratory or animal studies, with more limited evidence in humans
In addition, a direct and specific increase of CPT1A in HepG2 cells plays a crucial role in the lipid-lowering and anti-inflammatory effects exerted by Ginkgo biloba extract, quercetin, kaempferol, and isorhamnetin (Wei et al., 2014)
Another possible strategy to delay aging is to express a lysosome-targeted transmembrane proton-motive force-driven transhydrogenase, such as a mammalian NNT homolog, with the nucleotide binding domain facing the cytoplasm (Figure 3B)
While our study is limited by a small sample size and retrospective data collection procedure, we nonetheless thoroughly investigated clinical and biochemical data and compared the clinical features of euDKA and hyDKA
Collectively, these studies indicate that modulation of NAD + levels affects additional critical cellular pathways other than mitochondrial homeostasis
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