Cholesterol 6437 225755251 2008-07-15T06:55:49Z Jfdwolff 46555 rm original research - please only present content previously published in reliable sources {{Chembox new |ImageFile=Cholesterol.svg |ImageSize= |ImageFile2=Cholesterol-3d.png |IUPACName=(10R,13R)-10,13-dimethyl-17-(6-methylheptan-2-yl)- 2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H- cyclopenta[a]phenanthren-3-ol |OtherNames= |Section1= {{Chembox Identifiers | CASNo=57-88-5 | PubChem=5997 | SMILES=CC(C)CCCC(C)C1CCC2C1 (CCC3C2CC=C4C3(CCC(C4)O)C)C }} |Section2= {{Chembox Properties | Formula=C<sub>27</sub>H<sub>46</sub>O | MolarMass=386.654 | Appearance= white crystalline powder <ref name=MSDS>{{cite web |url=http://physchem.ox.ac.uk/MSDS/CH/cholesterol.html |title=Safety (MSDS) data for cholesterol |accessdate=2007-10-20 |format= |work=}}</ref> | Density= | MeltingPt=148–150 °C <ref name=MSDS/> | BoilingPt=360 °C (decomposes) | Solubility=0.095 mg/L (30 °C) }} |Section3= {{Chembox Hazards | MainHazards= | FlashPt= | Autoignition= }} }} [[Image:Adamantinomatous craniopharyngioma.jpg|thumb|200px|right|Microscopic appearance of cholesterol crystals in water. Photo taken under [[polarized light]].]] '''Cholesterol''' is a [[lipid]] found in the [[cell membrane]]s of all animal tissues, and is transported in the [[blood plasma]] of all [[animal]]s. Cholesterol is also a [[sterol]] (a combination [[steroid]] and [[alcohol]]). Because cholesterol is synthesized by all [[eukaryote]]s, trace amounts of cholesterol are also found in membranes of [[plant]]s and [[Fungus|fungi]]. The name originates from the [[Greek language|Greek]] ''chole-'' ([[bile]]) and ''stereos'' (solid), and the [[chemical]] [[suffix]] ''-ol'' for an alcohol, as researchers first identified cholesterol in solid form in [[gallstone]]s by François Poulletier de la Salle in [[1769]]. However, it is only in [[1815]] that chemist [[Michel Eugène Chevreul|Eugène Chevreul]] named the compound "cholesterine".<ref>{{cite journal |author=Olson RE |title=Discovery of the lipoproteins, their role in fat transport and their significance as risk factors |journal=J. Nutr. |volume=128 |issue=2 Suppl |pages=439S–443S |year=1998 |pmid=9478044 |url=http://jn.nutrition.org/cgi/content/full/128/2/439S}}</ref> Most of the cholesterol in the body is synthesized by the body and some has dietary origin. Cholesterol is more abundant in tissues which either synthesize more or have more abundant densely-packed membranes, for example, the [[liver]], [[spinal cord]] and [[brain]]. It plays a central role in many [[biochemistry|biochemical]] processes, such as the composition of [[cell membrane]]s and the synthesis of [[steroid hormone]]s.<ref>{{cite book |last=Stryer |first=Lubert |title=Biochemistry |edition=4th ed. |year=1995|publisher=W.H. Freeman & co. |location=New York |language=English |isbn=0-7167-2009-4 |pages= 280, 703}}</ref> Since cholesterol is insoluble in blood, it is transported in the circulatory system within [[lipoprotein]]s, complex spherical particles which have an exterior composed mainly of water-soluble proteins; [[lipid|fats]] and cholesterol are carried internally. There is a large range of lipoproteins within blood, generally called, from larger to smaller size: [[chylomicron]]s, [[very low density lipoprotein]] (VLDL), [[intermediate density lipoprotein]] (IDL), [[low density lipoprotein]] (LDL) and [[high density lipoprotein]] (HDL). The cholesterol within all the various lipoproteins is identical. According to the [[lipid hypothesis]], abnormally high cholesterol levels ([[hypercholesterolemia]]), or, more correctly, higher concentrations of LDL and lower concentrations of functional HDL are strongly associated with [[cardiovascular disease]] because these promote [[atheroma]] development in arteries ([[atherosclerosis]]). This disease process leads to [[myocardial infarction]] (heart attack), [[stroke]] and [[peripheral vascular disease]]. Since higher blood LDL, especially higher LDL particle concentrations and smaller LDL particle size, contribute to this process more than the cholesterol content of the LDL particles <ref name=Brun>{{cite journal |author=Brunzell JD ''et al'' |title=Consensus statement from the American Diabetes Association and the American College of Cardiology Foundation – Lipoprotein management in patients with cardiometabolic risk |journal=Diabetes Care | volume=31| number=4| pages=811–822| month=April| year=2008| pmid=18375431 |url=http://care.diabetesjournals.org/cgi/reprint/31/4/811 |doi=10.2337/dc08-9018}}</ref>, LDL particles are often termed "bad cholesterol" because they have been linked to atheroma formation. On the other hand, high concentrations of functional HDL, which can remove cholesterol from cells and atheroma, offer protection and are sometimes referred to colloquially as "good cholesterol". These balances are mostly genetically determined but can be changed by body build, [[medication]]s, food choices and other factors.<ref name="pmid12957096">{{cite journal |author=Durrington P |title=Dyslipidaemia |journal=Lancet |volume=362 |issue=9385 |pages=717–31 |year=2003 |pmid=12957096 |doi=10.1016/S0140-6736(03)14234-1}}</ref> ==Physiology== ===Function=== Cholesterol is required to build and maintain [[cell membrane]]s; it regulates membrane fluidity over a wide range of [[temperature]]s. The [[hydroxyl]] group on cholesterol interacts with the [[Polar_molecules|polar]] head groups of the [[Lipid Bilayer|membrane]] [[Phospholipid|phospho-]] and [[Sphingolipid|sphingolipids]], while the bulky [[steroid]] and the [[hydrocarbon]] chain is embedded in the membrane, alongside the [[Polar_molecules#Non-polar_molecules|nonpolar]] [[Fatty_acid|fatty acid chains]] of the other lipids. Some research indicates that cholesterol may act as an [[antioxidant]].<ref name=Smith1991>{{cite journal |author=Smith LL |title=Another cholesterol hypothesis: cholesterol as antioxidant |journal=Free Radic. Biol. Med. |volume=11 |issue=1 |pages=47–61 |year=1991 |pmid=1937129 |doi=}}</ref> Cholesterol also aids in the manufacture of [[bile]] (which is stored in the gallbladder and helps digest fats), and is also important for the metabolism of [[fat soluble vitamins]], including vitamins [[vitamin A|A]], [[vitamin D|D]], [[vitamin E|E]] and [[vitamin K|K]]. It is the major precursor for the synthesis of [[vitamin D]] and of the various [[steroid hormone]]s (which include [[cortisol]] and [[aldosterone]] in the [[adrenal gland]]s, and the sex hormones [[progesterone]], the various [[estrogen]]s, [[testosterone]], and derivatives). Recently, cholesterol has also been implicated in cell signaling processes, where it has been suggested that it assists in the formation of [[lipid rafts]] in the [[plasma membrane]]. It also reduces the permeability of the plasma membrane to [[hydrogen]] ions ([[proton]]s) and [[sodium ion]]s.<ref name=Haines2001>{{cite journal |author=Haines TH |title=Do sterols reduce proton and sodium leaks through lipid bilayers? |journal=Prog. Lipid Res. |volume=40 |issue=4 |pages=299–324 |year=2001 |pmid=11412894 |doi=}}</ref> Cholesterol is essential for the structure and function of invaginated [[caveolae]] and clathrin-coated pits, including the caveolae-dependent [[endocytosis]] and clathrin-dependent endocytosis. The role of cholesterol in caveolae-dependent and clathrin-dependent endocytosis can be investigated by using [[methyl beta cyclodextrin]] (MβCD) to remove cholesterol from the plasma membrane. ===Synthesis and intake=== [[Image:HMG-CoA reductase pathway.png|280px|thumb|right|The HMG-CoA reductase pathway]] Cholesterol is required in the membrane of mammalian cells for normal cellular function, and is either synthesized in the [[endoplasmic reticulum]], or derived from the diet, in which case it is delivered by the bloodstream in [[low-density lipoprotein]]s. These are taken into the cell by [[LDL receptor]]-mediated [[endocytosis]] in [[clathrin]]-[[coated pits]], and then hydrolysed in lysosomes. Cholesterol is primarily synthesized from [[acetyl CoA]] through the [[HMG-CoA reductase pathway]] in many [[cell (biology)|cells]] and [[biological tissue|tissues]]. About 20–25% of total daily production (~1 [[gram|g]]/[[day]]) occurs in the [[liver]]; other sites of higher synthesis rates include the [[intestines]], [[adrenal gland]]s and [[reproductive organ]]s. For a person of about {{convert|150|lb}}, typical total body content is about 35 g, typical daily internal production is about 1 g and typical daily dietary intake is 200–300 mg in the United States and societies adopting its dietary patterns. Of the cholesterol input to the intestines via bile production, 92–97% is reabsorbed in the intestines and recycled via [[enterohepatic circulation]]. [[Konrad Bloch]] and [[Feodor Lynen]] shared the [[Nobel Prize in Physiology or Medicine]] in 1964 for their discoveries concerning the mechanism and regulation of the cholesterol and [[fatty acid]] metabolism. ===Regulation=== Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the [[homeostasis|homeostatic]] mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, while lower intake from food has the opposite effect. The main regulatory mechanism is the sensing of [[intracellular]] cholesterol in the [[endoplasmic reticulum]] by the [[protein]] [[Sterol regulatory element binding protein|SREBP]] (Sterol Regulatory Element Binding Protein 1 and 2). In the presence of cholesterol, SREBP is bound to two other proteins: SCAP (SREBP-cleavage activating protein) and [[Insig1]]. When cholesterol levels fall, Insig-1 dissociates from the SREBP-SCAP complex, allowing the complex to migrate to the [[Golgi apparatus]], where SREBP is cleaved by S1P and S2P (site-1 and -2 protease), two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus and acts as a [[transcription factor]] to bind to the [[Sterol regulatory element|SRE]] (sterol regulatory element) of a number of genes to stimulate their [[Transcription (genetics)|transcription]]. Among the genes transcribed are the [[LDL receptor]] and [[HMG-CoA reductase pathway|HMG-CoA reductase]]. The former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol.<ref>{{cite journal | author=Brown MS, Goldstein JL | title=The SREBP pathway: regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor | year=1997 | journal=Cell | volume=89 | pages=331 | pmid=9150132 | doi=10.1016/S0092-8674(00)80213-5 | url=http://www.cell.com/content/article/abstract?uid=PIIS0092867400802135}}</ref> A large part of this mechanism was clarified by Dr. [[Michael S. Brown]] and Dr. [[Joseph L. Goldstein]] in the 1970s. In 1985, they received the [[Nobel Prize in Physiology or Medicine]] for their work. ===Excretion=== Cholesterol is excreted from the [[liver]] in [[bile]] and reabsorbed from the intestines. Under certain circumstances, when more concentrated, as in the [[gallbladder]], it crystallises and is the major constituent of most [[gallstone]]s, although [[lecithin]] and [[bilirubin]] gallstones also occur less frequently. ===In blood=== {{Seealso|Blood lipids}} Cholesterol is minimally soluble in [[water]]; it cannot dissolve and travel in the water-based bloodstream. Instead, it is transported in the bloodstream by [[lipoprotein]]s—protein "molecular-suitcases" that are water-soluble and carry cholesterol and [[triglyceride]]s internally. The [[apolipoprotein]]s forming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed and to where it will be supplied. Cholesterol is transported towards peripheral tissues by the lipoproteins [[chylomicrons]], [[very low density lipoprotein]]s (VLDL) and [[low-density lipoprotein]]s (LDL). Large numbers of small dense LDL (sdLDL) particles are strongly associated with the presence of [[atheroma]]tous disease within the arteries. For this reason, LDL is referred to as "bad cholesterol". On the other hand, [[high-density lipoprotein]] (HDL) particles transport cholesterol back to the liver for excretion. Having large numbers of large HDL particles correlates with better health outcomes, and hence it is commonly called "good cholesterol". In contrast, having small amounts of large HDL particles is independently associated with [[atheroma]]tous disease progression within the arteries. ==Clinical significance== ===Hypercholesterolemia=== {{main|hypercholesterolemia|lipid hypothesis}} Conditions with elevated concentrations of oxidized LDL particles, especially "small dense LDL" (sdLDL) particles, are associated with [[atheroma]] formation in the walls of [[artery|arteries]], a condition known as ''[[atherosclerosis]]'', which is the principal cause of [[coronary heart disease]] and other forms of [[cardiovascular disease]]. In contrast, HDL particles (especially large HDL) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma. Increased concentrations of HDL correlate with lower rates of atheroma progressions and even regression. A 2007 study pooling data on almost 900,000 subjects in 61 cohorts demonstrated that blood total cholesterol levels have an exponential effect on cardiovascular and total mortality, with the association more pronounced in younger subjects. Still, because cardiovascular disease is relatively rare in the younger population, the impact of high cholesterol on health is still larger in older people.<ref name=PSC>{{cite journal |author=Lewington S, Whitlock G, Clarke R, ''et al'' |title=Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths |journal=Lancet |volume=370 |issue=9602 |pages=1829–39 |year=2007 |month=December |pmid=18061058 |doi=10.1016/S0140-6736(07)61778-4}}</ref> There remains some opposition to the link between cholesterol and [[coronary heart disease]], termed the "[[lipid hypothesis]]".{{fact|date=May 2008}} Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL are regarded as ''atherogenic'' (prone to cause atherosclerosis).{{fact|date=March 2007}} Levels of these fractions, rather than the total cholesterol level, correlate with the extent and progress of atherosclerosis. Conversely, the total cholesterol can be within normal limits, yet be made up primarily of small LDL and small HDL particles, under which conditions atheroma growth rates would still be high. In contrast, however, if LDL particle number is low (mostly large particles) and a large percentage of the HDL particles are large, then atheroma growth rates are usually low, even negative, for any given total cholesterol concentration.{{Fact|date=February 2007}} Recently, a post-hoc analysis of the IDEAL and the EPIC prospective studies found an association between high levels of HDL cholesterol (adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the cardioprotective role of "good cholesterol".<ref>{{cite journal |author=van der Steeg WA |title=High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A-I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies |journal=J Am Coll Cardiol. |volume=51 |issue=6 |pages=634–642 |year=2008 |pmid=18261682 |doi=10.1016/j.jacc.2007.09.060}}</ref> Multiple human trials utilizing HMG-CoA reductase inhibitors, known as [[statins]], have repeatedly confirmed that changing lipoprotein transport patterns from unhealthy to healthier patterns significantly lowers cardiovascular disease event rates, even for people with cholesterol values currently considered low for adults. As a result, people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels,<ref>{{cite journal |author= |title=MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial |journal=Lancet |volume=360 |issue=9326 |pages=7–22 |year=2002 |pmid=12114036 |doi=}}</ref> and in men without cardiovascular disease there is benefit from lowering abnormally high cholesterol levels ("primary prevention").<ref>{{cite journal |author=Shepherd J, Cobbe SM, Ford I, ''et al'' |title=Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group |journal=N. Engl. J. Med. |volume=333 |issue=20 |pages=1301–7 |year=1995 |pmid=7566020 |doi=}}</ref> Primary prevention in women is practiced only by extension of the findings in studies on men,<ref>{{cite journal |author=Grundy SM |title=Should women be offered cholesterol lowering drugs to prevent cardiovascular disease? Yes |journal=BMJ |volume=334 |issue=7601 |pages=982 |year=2007 |pmid=17494017 |doi=10.1136/bmj.39202.399942.AD}}</ref> since in women, none of the large statin trials has shown a reduction in overall mortality or in cardiovascular end points.<ref>{{cite journal |author=Kendrick M |title=Should women be offered cholesterol lowering drugs to prevent cardiovascular disease? No |journal=BMJ |volume=334 |issue=7601 |pages=983 |year=2007 |pmid=17494018 |doi=10.1136/bmj.39202.397488.AD}}</ref> The 1987 report of [[National Cholesterol Education Program]], Adult Treatment Panels suggest the total blood cholesterol level should be: < 200 mg/dL normal blood cholesterol, 200–239 mg/dL borderline-high, > 240 mg/dL high cholesterol.<ref>{{cite journal |author= |title=Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel |journal=Arch. Intern. Med. |volume=148 |issue=1 |pages=36–69 |year=1988 |pmid=3422148 |doi=}}</ref>. The [[American Heart Association]] provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease:<ref name=AHA>[http://www.americanheart.org/cholesterol/about.jsp "About cholesterol"] – American Heart Association</ref> {| cellpadding=3 cellspacing=0 border=1 style="border-collapse:collapse" |bgcolor="#cccccc"| '''Level''' [[Milligram|mg]]/[[Decilitre|dL]] |bgcolor="#cccccc"| '''Level''' [[Mole (unit)|mmol]]/[[Litre|L]] |bgcolor="#cccccc"| '''Interpretation''' |- | < 200 | < 5.2 | Desirable level corresponding to lower risk for heart disease |- | 200–240 | 5.2–6.2 | Borderline high risk |- | > 240 | > 6.2 | High risk |} However, as today's testing methods determine LDL ("bad") and HDL ("good") cholesterol separately, this simplistic view has become somewhat outdated. The desirable LDL level is considered to be less than 100 mg/dL (2.6 [[Mole (unit)|mmol]]/L)<ref name=AHA>[http://www.americanheart.org/cholesterol/about.jsp "About cholesterol"] – American Heart Association</ref>, although a newer target of < 70 mg/dL can be considered in higher risk individuals based on some of the above-mentioned trials. A ratio of total cholesterol to HDL—another useful measure—of far less than 5:1 is thought to be healthier. Of note, typical LDL values for children before [[fatty streaks]] begin to develop is 35 mg/dL. Most testing methods for LDL do not actually measure LDL in their blood, much less particle size. For cost reasons, LDL values have long been estimated using the Friedewald formula: [total cholesterol] − [total HDL] − 20% of the [[triglyceride]] value = estimated LDL. The basis of this is that Total cholesterol is defined as the sum of HDL, LDL, and VLDL. Ordinarily just the total, HDL, and triglycerides are actually measured. The VLDL is estimated as one-fifth of the triglycerides. It is important to fast for at least eight hours before the blood test because the triglyceride level varies significantly with food intake. Given the well-recognized role of cholesterol in cardiovascular disease, it is surprising that some studies have shown an inverse correlation between cholesterol levels and mortality in subjects over 50 years of age—an 11% increase overall and 14% increase in CVD mortality per 1 mg/dL per year drop in cholesterol levels. In the [[Framingham Heart Study]], the researchers attributed this phenomenon to the fact that people with severe chronic diseases or cancer tend to have below-normal cholesterol levels.<ref name=Anderson1987>{{cite journal |author=Anderson KM., Castelli WP, Levy D. |title=Cholesterol and mortality. 30 years of follow-up from the Framingham study |journal=JAMA |volume=257 |pages=2176–80 |year=1987 |pmid=3560398 |doi=10.1001/jama.257.16.2176}}</ref> This explanation is not supported by the Vorarlberg Health Monitoring and Promotion Programme, in which men of all ages and women over 50 with very low cholesterol were increasingly likely to die of cancer, liver diseases, and mental diseases. This result indicates that the low cholesterol effect occurs even among younger respondents, contradicting the previous assessment among cohorts of older people that this is a proxy or marker for frailty occurring with age.<ref name=Ulmer2004>{{cite journal |author=Ulmer H., Kelleher C., Diem G., Concin H. |title=Why Eve is not Adam: prospective follow-up in 149650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality |journal=J Women's Health (Larchmt) |volume=13 |pages=41–53 |year=2004 |pmid=15006277 | doi = 10.1089/154099904322836447 <!--Retrieved from PMID by DOI bot-->}}</ref> A small group of scientists, united in [[The International Network of Cholesterol Skeptics]], continues to question the link between cholesterol and atherosclerosis.<ref>{{cite book |author=Uffe Ravnskov |title=The Cholesterol Myths : Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease |publisher=New Trends Publishing, Incorporated |location= |year= |pages= |isbn=0-96708-970-0 |oclc= |doi=}}</ref> However, the vast majority of doctors and medical scientists accepts the link as fact.<ref>{{cite book |author=Daniel Steinberg |title=The Cholesterol Wars: The Cholesterol Skeptics vs the Preponderance of Evidence |publisher=Academic Press |location=Boston |year= |pages= |isbn=0-12-373979-9 |oclc= |doi=}}</ref> ===Hypocholesterolemia=== Abnormally low levels of cholesterol are termed ''[[hypocholesterolemia]]''. Research into the causes of this state is relatively limited, but some studies suggest a link with [[depression (mood)|depression]], [[cancer]] and [[cerebral hemorrhage]]. Generally, the low cholesterol levels seem to be a consequence of an underlying illness, rather than a cause.<ref name=PSC/> ===Cholesterol testing=== It is recommended by the [[American Heart Association]] to test cholesterol every 5 years for people aged 20 years or older. <ref>{{cite web|author=American Heart Association| title= How To Get Your Cholesterol Tested| url= http://www.americanheart.org/presenter.jhtml?identifier=541}}</ref> A blood sample taken after fasting is taken by a doctor or a home cholesterol monitoring device to determine a lipoprotein profile. This measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol and triglycerides. It is recommended to have cholesterol tested more frequently than 5 years if a person: has total cholesterol of 200 mg/dL or more, is a man over age 45 or a woman over age 50, has HDL (good) cholesterol less than 40 mg/dL, or other risk factors for heart disease and stroke. ==Food sources== Cholesterol is found in animal fats: all food containing animal fats contains cholesterol; food not containing animal fats either contains no cholesterol or negligible amounts. Major dietary sources of cholesterol include egg yolks, beef, poultry, and shrimp.<ref>[http://www.health.gov/dietaryguidelines/dga2005/report/HTML/table_e18.htm Nutrition and Your Health: Dietary Guidelines for Americans. Table E-18. Dietary Sources of Cholesterol Listed in Decreasing Order.]</ref> Human [[breast milk]] also contains significant quantities of cholesterol.<ref name=ajcn-breastmilk>{{cite journal | author=Jensen RG, Hagerty MM, McMahon KE | title=Lipids of human milk and infant formulas: a review | journal=Am J Clin Nutr | year=1978 | pages=990-1016 | volume=31 | pmid=352132 | url=http://www.ajcn.org/cgi/reprint/31/6/990 | format=PDF}}</ref> Plants have trace amounts of cholesterol, so even a [[vegan]] diet, which includes no animal foods, has traces of cholesterol. However, the amounts are very small. For example, to ingest the amount of cholesterol in one egg yolk, one would need to drink about {{convert|9.6|L}} of pure peanut oil.<ref name=AHA>[http://www.americanheart.org/cholesterol/about.jsp "About cholesterol"] – American Heart Association</ref> <ref name=behrman2005>Behrman EJ, Gopalan V. Cholesterol and plants. ''J Chem Educ'' 2005;82:1791–1793. [http://jchemed.chem.wisc.edu/HS/Journal/Issues/2005/Dec/clicSubscriber/V82N12/p1791.pdf PDF]</ref> Plant products (e.g. [[flax seed]], [[peanut]]), also contain cholesterol-like compounds, [[phytosterols]], which are suggested to help lower [[serum]] cholesterol.<ref name=ostlund2003>{{cite journal | author=Ostlund RE, Racette, SB, and Stenson WF | title=Inhibition of cholesterol absorption by phytosterol-replete wheat germ compared with phytosterol-depleted wheat germ | journal=Am J Clin Nutr | year=2003 | pages=1385–1589 | volume=77 | issue=6 |pmid=12791614}}</ref> ==Cholesteric liquid crystals== Some cholesterol derivatives, (among other simple cholesteric lipids) are known to generate the [[liquid crystal]]line ''cholesteric phase''. The cholesteric phase is in fact a [[chirality (chemistry)|chiral]] [[Liquid crystal|nematic phase]], and changes colour when its temperature changes. Therefore, cholesterol derivatives are commonly used in liquid crystal [[thermometer]]s and temperature-sensitive paints. ==See also== * [[Triglyceride]]s * [[Diet and heart disease]] * [[Bile salts]] *[[Lieberman-Burchard test]] ==Additional images== <gallery> Image:Steroidogenesis.gif|[[Steroidogenesis]] Image:Cholesterol_Spacefill.jpeg|[[Space-filling model]] of the Cholesterol molecule Image:Steroid-nomenclature.png|Numbering of the [[steroid]] nucleus </gallery> ==Footnotes== {{Reflist|2}} ==External links== * [http://www.nhlbi.nih.gov/guidelines/cholesterol/ Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults] US National Institutes of Health Adult Treatment Panel III * [http://www.fao.org/docrep/V4700E/V4700E08.htm Aspects of fat digestion and metabolism – UN/WHO Report 1994] * [http://www.americanheart.org/cholesterol/about.jsp American Heart Association] – "About Cholesterol" {{Sterols}} [[Category:Steroids]] [[Category:Sterols]] [[Category:Lipid disorders]] [[Category:Nutrition]] {{Link FA|ja}} [[ar:كولسترول]] [[az:Xolesterin]] [[bg:Холестерол]] [[ca:Colesterol]] [[cs:Cholesterol]] [[da:Kolesterol]] [[de:Cholesterin]] [[et:Kolesterool]] [[el:Χοληστερίνη]] [[es:Colesterol]] [[eo:Kolesterolo]] [[fa:کلسترول]] [[fr:Cholestérol]] [[gl:Colesterol]] [[ko:콜레스테롤]] [[hr:Kolesterol]] [[id:Kolesterol]] [[it:Colesterolo]] [[he:כולסטרול]] [[lt:Cholesterolis]] [[ml:കൊളസ്ട്രോള്‍]] [[ms:Kolesterol]] [[nl:Cholesterol]] [[ja:コレステロール]] [[no:Kolesterol]] [[oc:Colesteròl]] [[pl:Cholesterol]] [[pt:Colesterol]] [[ro:Colesterol]] [[ru:Холестерол]] [[sq:Kolesteroli]] [[simple:Cholesterol]] [[sk:Cholesterol]] [[sr:Холестерол]] [[fi:Kolesteroli]] [[sv:Kolesterol]] [[th:คอเลสเตอรอล]] [[vi:Cholesterol]] [[tr:Kolesterol]] [[uk:Холестерин]] [[zh-yue:膽固醇]] [[zh:膽固醇]]