PPARγ regulates adipocyte cholesterol metabolism via oxidized LDL receptor 1

In addition to its role in energy storage, adipose tissue also accumulates cholesterol. Concentrations of cholesterol and triglycerides are strongly correlated in the adipocyte, but little is known about mechanisms regulating cholesterol metabolism in fat cells. Here we report that antidiabetic thiazolidinediones (TZDs) and other ligands for the nuclear receptor PPARγ dramatically upregulate oxidized LDL receptor 1 (OLR1) in adipocytes by facilitating the exchange of coactivators for corepressors on the OLR1 gene in cultured mouse adipocytes. TZDs markedly stimulate the uptake of oxidized LDL (oxLDL) into adipocytes, and this requires OLR1. Increased OLR1 expression, resulting either from TZD treatment or adenoviral gene delivery, significantly augments adipocyte cholesterol content and enhances fatty acid uptake. OLR1 expression in white adipose tissue is increased in obesity and is further induced by PPARγ ligand treatment in vivo. Serum oxLDL levels are decreased in both lean and obese diabetic animals treated with TZDs. These data identify OLR1 as a novel PPARγ target gene in adipocytes. While the physiological role of adipose tissue in cholesterol and oxLDL metabolism remains to be established, the induction of OLR1 is a potential means by which PPARγ ligands regulate lipid metabolism and insulin sensitivity in adipocytes

NA62 results on Dark Sector searches

NA62 is a precision physics experiment studying charged kaons and their decayproducts with an unprecedented accuracy (measurement of the K + → π + ννbranching ratio of the order of 10 −11), allowing indirect probes of new physicsscales up to O(100) TeV. NA62 experiment also searches directly for weaklyinteracting particles of up to O(100) MeV masses in kaon decays and up to O(1)GeV masses when running in the beam dump mode. For both modes of directsearches, NA62 has been collecting data since 2021 after a successful 2016-18run 1. Past results and future prospects are presented in this talk