Min Sun Kim

TL;DR: APR-induced alterations initially protect the host from the harmful effects of bacteria, viruses, and parasites, however, if prolonged, these changes in the structure and function of lipoproteins will contribute to atherogenesis.

TL;DR: It is demonstrated that tumor necrosis factor (TNF) and interleukin 1 (IL-1), but not IL-6, decrease the expression of retinoid X receptor alpha (RXRalpha), peroxisome proliferator-activated receptoralpha (PPARalpha), PPARgamma, liver X receptoralpha, and coactivator 1 (SRC-1) in Hep3B human hepatoma cells.

TL;DR: It is shown that LPS significantly decreases farnesoid X receptor (FXR) mRNA in mouse liver as early as 8 h after LPS administration, and this decrease was dose-dependent with the half-maximal effect observed at 0.5 μg/100 g of body weight.

TL;DR: It is demonstrated that LPS treatment produces a rapid and marked decrease in the mRNA levels of all three RXR isoforms, PPARalpha and PPARdelta, and TRalpha and TRbeta in the heart, which could account for the decreased expression of key proteins required for fatty acid oxidation and thereby play an important role in cardiac contractility.

TL;DR: The results suggest that decreased levels or activities of FXR, PXR, and CAR during the APR could contribute to decreases in Sult2A1, resulting in decreased sulfation of DHEA and lower circulating level of D HEA-S.