Metabolism


Serine/threonine kinase AMPK upregulates glucose uptake by promoting the expression and function of glucose transporters. AMPK is activated by increased AMP/ATP ratio, resulting from cellular and environmental stress, e.g. low glucose, heat shock, hypoxia and ischemia. AMPK activation positively modulates signaling transductions that refill ATP levels. Moreover, it also stimulates catabolic processes such as fatty acid oxidation and glycolysis through inhibition of ACC and activation of PFK2. AMPK negatively regulates various proteins which are important to ATP-consuming mechanisms, e.g. mTORC2, glycogen synthase, SREBP-1, and TSC2, causing the downregulation/inhibition of gluconeogenesis and glycogen, lipid and protein synthesis.
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C5619 N-BenzylpalmitamideSummary: inhibitor of fatty acid amide hydrolase (FAAH) -
C5631 Glycerophospho-N-Oleoyl EthanolamineSummary: precursor of oleoyl ethanolamide (OEA) -
C5603 A-771726Summary: dihydroorotate dehydrogenase inhibitor -
C5712 DG-172 (hydrochloride)Summary: orally available inverse agonist of PPARβ/δ -
C5478 NCT-502Summary: inhibitor of 3-phosphoglycerate dehydrogenase (PHGDH) -
C5557 SR 1824Summary: non-agonist PPARγ ligand -
C5435 G3335Summary: PPARγ antagonist -
C5572 SR 2595Summary: inverse agonist of PPARγ -
C5491 trans-AUCBSummary: potent inhibitor of soluble epoxide hydrolase (sEH) -
C5452 Monoacylglycerol Lipase Inhibitor 21Summary: inhibitor of monoacylglycerol lipase (MAGL) and FAAH

