17β-HSD13 Activators interact with various aspects of cellular metabolism that are critical to the functioning and regulation of 17β-HSD13. These compounds generally target signaling pathways and metabolic processes that are crucial for the homeostasis of lipids and steroids within the cell. For instance, activators of PPARs, such as Pioglitazone, Bezafibrate, GW501516, Rosiglitazone, and Fenofibrate, modulate gene expression profiles that govern lipid metabolism, which could lead to an upregulation of 17β-HSD13 as the enzyme plays a role in these metabolic pathways. On the other hand, compounds like Forskolin and AICAR engage with secondary messenger systems and cellular energy sensors, respectively, to potentially alter the cellular metabolic state, thereby impacting the activity of 17β-HSD13.
Moreover, metabolic intermediates and cofactors such as NAD+ and L-Carnitine are involved in fundamental processes that could modulate 17β-HSD13 indirectly. NAD+, a vital redox cofactor, is central to the metabolism of fatty acids and steroids, which are substrates and products of 17β-HSD13's enzymatic activity. Similarly, L-Carnitine's role in fatty acid transport into mitochondria can influence β-oxidation processes, potentially increasing the substrate availability for enzymes like 17β-HSD13. The presence of specific bile acids like Cholic Acid and Allocholic acid, known to participate in the emulsification and breakdown of fats, suggests a milieu that may necessitate the activity of enzymes involved in lipid processing, including 17β-HSD13.
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