LLight
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- Joined
- May 30, 2018
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- 1,411
Do they do that incidentally or by design? My understanding is they are always undesirable and are a major cause of arteriosclerosis.
I'm not really knowledgeable about this topic . Maybe the confusion might be due to the fact that oxysterols are a class of compounds which may have different impacts on the body (in addition to the potential activation of the LXR).
My "claims" were based on these publications:
4β-Hydroxycholesterol Signals From the Liver to Regulate Peripheral Cholesterol Transporters
"Like many other oxysterols, 4β-hydroxycholesterol (4βHC) is a ligand for liver X receptors (LXRs), the major regulators of lipid metabolism (Janowski et al., 1996; Lee and Tontonoz, 2015). Both LXRα (NR1H3) and LXRβ (NR1H2) are activated by 4βHC to a similar degree in vitro (Nury et al., 2013), but the role of 4βHC in the regulation of LXR targets is yet to be explored. LXRα is expressed in the liver, intestine, kidney, adipose tissue, adrenals, and macrophages, while LXRβ is expressed ubiquitously (Lee and Tontonoz, 2015). The activation of LXR leads to upregulation of lipogenesis in the liver and induction of cholesterol efflux transporters such as ATP-binding cassette transporters A1 (ABCA1), ABCG1, and ABCG5/8, as well as repression of LDL receptor-mediated lipoprotein uptake in the liver and macrophages via inducible degrader of the LDL receptor (IDOL) (Lee and Tontonoz, 2015). The activation of LXR is generally considered to reduce atherosclerosis, while the induction of hepatic lipogenesis may lead to hepatosteatosis (Lee and Tontonoz, 2015)."
Transcriptional integration of metabolism by the nuclear sterol-activated receptors LXR and FXR
" Furthermore, in the liver, LXR promotes cholesterol conversion to bile acids by cytochrome P450 7A1 (CYP7A1)."
The Liver X-receptor Alpha Controls Hepatic Expression of the Human Bile Acid-Glucuronidating UGT1A3 Enzyme in Human Cells and Transgenic Mice - PubMed
"Glucuronidation, an important bile acid detoxification pathway, is catalyzed by enzymes belonging to the UDP-glucuronosyltransferase (UGT) family. Among UGT enzymes, UGT1A3 is considered the major human enzyme for the hepatic C24-glucuronidation of the primary chenodeoxycholic (CDCA) and secondary lithocholic (LCA) bile acids. We identify UGT1A3 as a positively regulated target gene of the oxysterol-activated nuclear receptor liver X-receptor alpha (LXRalpha)."