Editing Cholesterol (section)

===Metabolism, recycling and excretion===
Cholesterol is susceptible to oxidation and easily forms oxygenated derivatives called [[oxysterol]]s. Three different mechanisms can form these: autoxidation, secondary oxidation to lipid peroxidation, and cholesterol-metabolizing enzyme oxidation. A great interest in oxysterols arose when they were shown to exert inhibitory actions on cholesterol biosynthesis.<ref name="Kandutsch_1978">{{cite journal | vauthors = Kandutsch AA, Chen HW, Heiniger HJ | title = Biological activity of some oxygenated sterols | journal = Science | volume = 201 | issue = 4355 | pages = 498–501 | date = August 1978 | pmid = 663671 | doi = 10.1126/science.663671 | bibcode = 1978Sci...201..498K }}</ref> This finding became known as the "oxysterol hypothesis". Additional roles for oxysterols in human physiology include their participation in bile acid biosynthesis, function as transport forms of cholesterol, and regulation of gene transcription.<ref name="Russell_2000">{{cite journal | vauthors = Russell DW | title = Oxysterol biosynthetic enzymes | journal = Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids | volume = 1529 | issue = 1–3 | pages = 126–35 | date = December 2000 | pmid = 11111082 | doi = 10.1016/S1388-1981(00)00142-6 }}</ref>

In biochemical experiments, radiolabelled forms of cholesterol, such as tritiated-cholesterol, are used. These derivatives undergo degradation upon storage, and it is essential to purify cholesterol prior to use. Cholesterol can be purified using small Sephadex LH-20 columns.<ref name="Hanukoglu_1980">{{cite journal | vauthors = Hanukoglu I, Jefcoate CR | title = Pregnenolone separation from cholesterol using Sephadex LH-20 mini-columns|journal=Journal of Chromatography A | volume = 190 | issue = 1 | year = 1980 | pages = 256–262 | doi = 10.1016/S0021-9673(00)85545-4 | url = https://zenodo.org/record/890904 }}</ref>

Cholesterol is oxidized by the liver into a variety of [[bile acids]].<ref name="Javitt_1994">{{cite journal | vauthors = Javitt NB | title = Bile acid synthesis from cholesterol: regulatory and auxiliary pathways | journal = FASEB Journal | volume = 8 | issue = 15 | pages = 1308–1311 | date = December 1994 | pmid = 8001744 | doi = 10.1096/fasebj.8.15.8001744 | doi-access = free | s2cid = 20302590 }}</ref> These, in turn, are [[phase 2 reaction|conjugated]] with [[glycine]], [[taurine]], [[glucuronic acid]], or [[sulfate]]. A mixture of conjugated and nonconjugated bile acids, along with cholesterol itself, is excreted from the [[liver]] into the [[bile]]. Approximately 95% of the bile acids are reabsorbed from the intestines, and the remainder are lost in the feces.<ref name="Wolkoff_2003">{{cite journal | vauthors = Wolkoff AW, Cohen DE | title = Bile acid regulation of hepatic physiology: I. Hepatocyte transport of bile acids | journal = American Journal of Physiology. Gastrointestinal and Liver Physiology | volume = 284 | issue = 2 | pages = G175–G179 | date = February 2003 | pmid = 12529265 | doi = 10.1152/ajpgi.00409.2002 }}</ref> The excretion and reabsorption of bile acids forms the basis of the [[enterohepatic circulation]], which is essential for the digestion and absorption of dietary fats. Under certain circumstances, when more concentrated, as in the [[gallbladder]], cholesterol crystallises and is the major constituent of most [[gallstone]]s ([[lecithin]] and [[bilirubin]] gallstones also occur, but less frequently).<ref name="Marschall_2007">{{cite journal | vauthors = Marschall HU, Einarsson C | title = Gallstone disease | journal = Journal of Internal Medicine | volume = 261 | issue = 6 | pages = 529–542 | date = June 2007 | pmid = 17547709 | doi = 10.1111/j.1365-2796.2007.01783.x | s2cid = 8609639 | doi-access = free }}</ref> Every day, up to 1 g of cholesterol enters the colon. This cholesterol originates from the diet, bile, and desquamated intestinal cells, and it can be metabolized by the colonic bacteria. Cholesterol is converted mainly into [[coprostanol]], a nonabsorbable sterol that is excreted in the feces.{{citation needed|date=March 2019}}

Although cholesterol is a steroid generally associated with mammals, the human pathogen ''[[Mycobacterium tuberculosis]]'' is able to completely degrade this molecule and contains a large number of genes that are regulated by its presence.<ref>{{cite journal | vauthors = Wipperman MF, Sampson NS, Thomas ST | title = Pathogen roid rage: cholesterol utilization by Mycobacterium tuberculosis | journal = Critical Reviews in Biochemistry and Molecular Biology | volume = 49 | issue = 4 | pages = 269–293 | date = 2014 | pmid = 24611808 | pmc = 4255906 | doi = 10.3109/10409238.2014.895700 }}</ref> Many of these cholesterol-regulated genes are [[Homology (biology)|homologues]] of [[fatty acid]] [[β-oxidation]] genes, but have evolved in such a way as to bind large steroid substrates like cholesterol.<ref>{{cite journal | vauthors = Thomas ST, Sampson NS | title = Mycobacterium tuberculosis utilizes a unique heterotetrameric structure for dehydrogenation of the cholesterol side chain | journal = Biochemistry | volume = 52 | issue = 17 | pages = 2895–2904 | date = April 2013 | pmid = 23560677 | pmc = 3726044 | doi = 10.1021/bi4002979 }}</ref><ref>{{cite journal | vauthors = Wipperman MF, Yang M, Thomas ST, Sampson NS | title = Shrinking the FadE proteome of Mycobacterium tuberculosis: insights into cholesterol metabolism through identification of an α2β2 heterotetrameric acyl coenzyme A dehydrogenase family | journal = Journal of Bacteriology | volume = 195 | issue = 19 | pages = 4331–4341 | date = October 2013 | pmid = 23836861 | pmc = 3807453 | doi = 10.1128/JB.00502-13 }}</ref>