The novel SPPARM YR3-16 ameliorates metabolic disorders in vivo and attenuates adipocyte inflammation in vitro via PPARγ-dependent ERK suppression. (PubMed, Int Immunopharmacol)
YR3-16 is a novel tetrahydroisoquinoline derivative that selectively activates PPARγ and exhibits a binding mode distinct from that of pioglitazone...In 3 T3-L1 adipocytes, YR3-16 (10 μM) reprogrammed lipid metabolism at the gene transcriptional level, and suppressed pro-inflammatory cytokine secretion (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β)), associated with the inhibition of extracellular signal-regulated kinase (ERK) signaling pathway, which was abolished by the peroxisome proliferator-activated receptor γ antagonist GW9662. YR3-16, as a novel SPPARM, concurrently improves metabolic disorders in vivo and attenuates adipocyte inflammation via peroxisome proliferator-activated receptor γ activation, highlighting its potential for treating obesity-related diseases.