血清コレステロール

WordNet

an animal sterol that is normally synthesized by the liver; the most abundant steroid in animal tissues (同)cholesterin
an amber, watery fluid, rich in proteins, that separates out when blood coagulates (同)blood_serum

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コレステロール(胆汁・血液・神経組織などの脂肪性成分)
リンパ液 / 血清
serial / series / sermon

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/04/21 18:30:46」(JST)

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Microscopic appearance of cholesterol crystals in water. Photo taken under polarized light.

Cholesterol, from the Greek chole- (bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol, is an organic chemical substance classified as a waxy steroid of fat. It is an essential structural component of mammalian cell membranes and is required to establish proper membrane permeability and fluidity. In addition, cholesterol is an important component for the manufacture of bile acids, steroid hormones, and vitamin D. Cholesterol is the principal sterol synthesized by animals; in vertebrates it is formed predominantly in the liver. Small quantities are synthesized in other eukaryotes such as plants and fungi. It is almost completely absent among prokaryotes, i.e. bacteria.

Although cholesterol is important and necessary for human health, high levels of cholesterol in the blood have been linked to damage to arteries and cardiovascular disease.^[2]

François Poulletier de la Salle first identified cholesterol in solid form in gallstones, in 1769. However, it was only in 1815 that chemist Eugène Chevreul named the compound "cholesterine".^[3]

1 Physiology
- 1.1 Function
- 1.2 Dietary sources
- 1.3 Biosynthesis
- 1.4 Regulation of cholesterol synthesis
- 1.5 Plasma transport and regulation of absorption
- 1.6 Metabolism, recycling and excretion
2 Significance
- 2.1 Hypercholesterolemia
- 2.2 Hypocholesterolemia
- 2.3 Cholesterol testing
3 Interactive pathway map
4 Cholesteric liquid crystals
5 See also
6 Additional images
7 References
8 External links

Physiology

Since cholesterol is essential for all animal life, it is primarily synthesized from simpler substances within the body. However, high levels in blood circulation, depending on how it is transported within lipoproteins, are strongly associated with progression of atherosclerosis. For a person of about 68 kg (150 pounds), typical total body cholesterol synthesis is about 1 g (1,000 mg) per day, and total body content is about 35 g. Typical daily additional dietary intake in the United States is 200–300 mg.^[4] The body compensates for cholesterol intake by reducing the amount synthesized.^[5]

Cholesterol is recycled. It is excreted by the liver via the bile into the digestive tract. Typically about 50% of the excreted cholesterol is reabsorbed by the small bowel back into the bloodstream. Phytosterols can compete with cholesterol reabsorption in the intestinal tract, thus reducing cholesterol reabsorption.^[6]

Function

Cholesterol is required to build and maintain membranes; it modulates membrane fluidity over the range of physiological temperatures. The hydroxyl group on cholesterol interacts with the polar head groups of the membrane phospholipids and sphingolipids, while the bulky steroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty acid chain of the other lipids. Through the interaction with the phospholipid fatty acid chains, cholesterol increases membrane packing, which reduces membrane fluidity.^[7] In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes,^[8] protons, (positive hydrogen ions) and sodium ions.^[9]

Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependent endocytosis. The role of cholesterol in such endocytosis can be investigated by using methyl beta cyclodextrin (MβCD) to remove cholesterol from the plasma membrane. Recently, cholesterol has also been implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane. Lipid raft formation brings receptor proteins in close proximity with high concentrations of second messenger molecules.^[10] In many neurons, a myelin sheath, rich in cholesterol, since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.^[11]

Within cells, cholesterol is the precursor molecule in several biochemical pathways. In the liver, cholesterol is converted to bile, which is then stored in the gallbladder. Bile contains bile salts, which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, A, D, E, and K. Cholesterol is an important precursor molecule for the synthesis of vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone, as well as the sex hormones progesterone, estrogens, and testosterone, and their derivatives.

Some research indicates cholesterol may act as an antioxidant.^[12]

Dietary sources

Animal fats are complex mixtures of triglycerides, with lesser amounts of phospholipids and cholesterol. As a consequence, all foods containing animal fat contain cholesterol to varying extents.^[13] Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, fish, and shrimp.^[14] Human breast milk also contains significant quantities of cholesterol.^[15]

From a dietary perspective, cholesterol is not found in significant amounts in plant sources.^[14]^[16] In addition, plant products such as flax seeds and peanuts contain cholesterol-like compounds called phytosterols, which are believed to compete with cholesterol for absorption in the intestines.^[17] Phytosterols can be supplemented through the use of phytosterol-containing functional foods or nutraceuticals that are widely recognized as having a proven LDL cholesterol-lowering efficacy.^[18] Current supplemental guidelines recommend doses of phytosterols in the 1.6-3.0 grams per day range (Health Canada, EFSA, ATP III,FDA) with a recent meta-analysis demonstrating an 8.8% reduction in LDL-cholesterol at a mean dose of 2.15 gram per day.^[19] However, the benefits of a diet supplemented with phytosterol has been questioned.^[20]^[21]

Total fat intake also plays a role in blood cholesterol levels. This effect is thought to come about by changes in the quantity of cholesterol and lipoproteins that are synthesized by the body. In particular, saturated, monounsaturated and polyunsaturated fats have been shown to increase HDL-based cholesterol levels, with saturated fats also increasing LDL-based cholesterol levels.^[22] Trans fats have been shown to reduce levels of HDL whilst increasing levels of LDL.^[23] Based on such evidence and evidence implicating low HDL and high LDL levels in cardiovascular disease (see Hypercholesterolemia), many health authorities advocate reducing LDL cholesterol through changes in diet in addition to other lifestyle modifications.^[2] The USDA for example recommends that those wishing to reduce their cholesterol through a change in diet should aim to consume less than 7% of their daily energy needs from saturated fat and fewer than 200 mg of cholesterol per day.^[24] An alternative view is that any reduction to dietary cholesterol intake could be counteracted by the organs compensating to try to keep blood cholesterol levels constant.^[25]

However, the The China Study uses epidemiological evidence to claim that casein raises blood cholesterol even more than the ingested saturated fat or cholesterol.^[26]

Biosynthesis

All animal cells manufacture cholesterol with relative production rates varying by cell type and organ function. About 20–25% of total daily cholesterol production occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands, and reproductive organs. Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. This step is the regulated, rate-limiting and irreversible step in cholesterol synthesis and is the site of action for the statin drugs (HMG-CoA reductase competitive inhibitors).

Mevalonate is then converted to 3-isopentenyl pyrophosphate in three reactions that require ATP. Mevalonate is decarboxylated to isopentenyl pyrophosphate, which is a key metabolite for various biological reactions. Three molecules of isopentenyl pyrophosphate condense to form farnesyl pyrophosphate through the action of geranyl transferase. Two molecules of farnesyl pyrophosphate then condense to form squalene by the action of squalene synthase in the endoplasmic reticulum. Oxidosqualene cyclase then cyclizes squalene to form lanosterol. Finally, lanosterol is then converted to cholesterol.^[27]

Konrad Bloch and Feodor Lynen shared the Nobel Prize in Physiology or Medicine in 1964 for their discoveries concerning the mechanism and regulation of cholesterol and fatty acid metabolism.

Regulation of cholesterol synthesis

Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the homeostatic mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, whereas 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 SREBP (sterol regulatory element-binding protein 1 and 2).^[28] 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), which stimulates the transcription of many genes. Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase. The former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol.^[29] A large part of this signaling pathway 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. Their subsequent work shows how the SREBP pathway regulates expression of many genes that control lipid formation and metabolism and body fuel allocation.

Cholesterol synthesis can be turned off when cholesterol levels are high, as well. HMG CoA reductase contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain. The membrane domain functions to sense signals for its degradation. Increasing concentrations of cholesterol (and other sterols) cause a change in this domain's oligomerization state, which makes it more susceptible to destruction by the proteosome. This enzyme's activity can also be reduced by phosphorylation by an AMP-activated protein kinase. Because this kinase is activated by AMP, which is produced when ATP is hydrolyzed, it follows that cholesterol synthesis is halted when ATP levels are low.^[30]

Plasma transport and regulation of absorption

Metabolism, recycling and excretion

Cholesterol is susceptible to oxidation and easily forms oxygenated derivatives known as oxysterols. 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.^[34] 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.^[35]

Cholesterol is oxidized by the liver into a variety of bile acids.^[36] These, in turn, are 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.^[37] 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 gallstones. Although, lecithin and bilirubin gallstones also occur, but less frequently.^[38] Every day, up to 1 g of cholesterol enters the colon. This cholesterol originates from the diet, bile, and desquamated intestinal cells, and can be metabolized by the colonic bacteria. Cholesterol is converted mainly into coprostanol, a nonabsorbable sterol that is excreted in the feces. A cholesterol-reducing bacterium origin has been isolated from human feces.^[39]^{[non-primary source needed]}

Significance

Hypercholesterolemia

Main articles: hypercholesterolemia and lipid hypothesis

According to the lipid hypothesis, abnormal cholesterol levels (hypercholesterolemia) — that is, 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 HDL particles,^[40] 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 as "good cholesterol". These balances are mostly genetically determined, but can be changed by body build, medications, food choices, and other factors.^[41]

Conditions with elevated concentrations of oxidized LDL particles, especially "small dense LDL" (sdLDL) particles, are associated with atheroma formation in the walls of 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.^[42]

Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL are regarded as atherogenic (prone to cause atherosclerosis).^[43] 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.^{[citation needed]} 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".^[44]

Elevated cholesterol levels are treated with a strict diet consisting of low saturated fat, trans fat-free, low cholesterol foods,^[45]^[46] often followed by one of various hypolipidemic agents, such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants.^[47] Extreme cases have previously been treated with partial ileal bypass surgery, which has now been superseded by medication. Apheresis-based treatments are still used for very severe hyperlipidemias that are either unresponsive to treatment or require rapid lowering of blood lipids.^{[citation needed]}

Multiple human trials using 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.^{[citation needed]} Studies have also found that statins reduce atheroma progression.^[48] As a result, people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels,^[49] and in men without cardiovascular disease, there is benefit from lowering abnormally high cholesterol levels ("primary prevention").^[50] Primary prevention in women is practiced only by extension of the findings in studies on men,^[51] since in women, none of the large statin trials has shown a reduction in overall mortality or in cardiovascular endpoints.^[52]

Level mg/dL	Level mmol/L	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

The 1987 report of National Cholesterol Education Program, Adult Treatment Panels suggests the total blood cholesterol level should be: < 200 mg/dL normal blood cholesterol, 200–239 mg/dL borderline-high, > 240 mg/dL high cholesterol.^[53] The American Heart Association provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease:^[54]

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 mmol/L),^[55] although a newer upper limit of 70 mg/dL (1.8 mmol/L) 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.^{[citation needed]}

Reference ranges for blood tests, showing usual, as well as optimal, levels of HDL, LDL and total cholesterol in mass and molar concentrations, is found in orange color at right, that is, among the blood constituents with the highest concentration.

Total cholesterol is defined as the sum of HDL, LDL, and VLDL. Usually, only the total, HDL, and triglycerides are measured. For cost reasons, the VLDL is usually estimated as one-fifth of the triglycerides and the LDL is estimated using the Friedewald formula (or a variant): estimated LDL = [total cholesterol] − [total HDL] − [estimated VLDL]. VLDL can be calculated by dividing total triglycerides by five. Direct LDL measures are used when triglycerides exceed 400 mg/dL. The estimated VLDL and LDL have more error when triglycerides are above 400 mg/dL.^[56]

Given the well-recognized role of cholesterol in cardiovascular disease, some studies have shown an inverse correlation between cholesterol levels and mortality. A 2009 study of patients with acute coronary syndromes found an association of hypercholesterolemia with better mortality outcomes.^[57] In the Framingham Heart Study, in subjects over 50 years of age, they found an 11% increase overall and 14% increase in cardiovascular disease mortality per 1 mg/dL per year drop in total cholesterol levels. The researchers attributed this phenomenon to the fact that people with severe chronic diseases or cancer tend to have below-normal cholesterol levels.^[58] 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 likely to die of cancer, liver diseases, and mental diseases. This result indicates 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.^[59]

The vast majority of doctors and medical scientists consider that there is a link between cholesterol and atherosclerosis as discussed above;^[60] a small group of scientists, united in The International Network of Cholesterol Skeptics, questions the link.^[61]

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, cancer, and cerebral hemorrhage. In general, the low cholesterol levels seem to be a consequence, rather than a cause, of an underlying illness.^[42]

Cholesterol testing

The American Heart Association recommends testing cholesterol every five years for people aged 20 years or older.^[62]

A blood sample after 12-hour fasting is taken by a doctor, or a home cholesterol-monitoring device is used to determine a lipoprotein profile. This measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol, and triglycerides. It is recommended to test cholesterol at least every five years if a person has total cholesterol of 200 mg/dL or more, or if a man over age 45 or a woman over age 50 has HDL (good) cholesterol less than 40 mg/dL, or there are other risk factors for heart disease and stroke. (In different countries measurements are given in mg/dL or mmol/L; 1 mmol/L is 38.665 mg/dL.)

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. ^[63]

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Statin Pathway edit

Cholesteric liquid crystals

Some cholesterol derivatives (among other simple cholesteric lipids) are known to generate the liquid crystalline "cholesteric phase". The cholesteric phase is, in fact, a chiral nematic phase, and it changes colour when its temperature changes. This makes cholesterol derivatives useful for indicating temperature in liquid crystal display thermometers and in temperature-sensitive paints.

Additional images

Steroidogenesis, using cholesterol as building material
Space-filling model of the Cholesterol molecule
Numbering of the steroid nuclei

References

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^ Durrington P (August 2003). "Dyslipidaemia". Lancet 362 (9385): 717–31. doi:10.1016/S0140-6736(03)14234-1. PMID 12957096.
^ ^a ^b Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, Halsey J, Qizilbash N, Peto R, Collins R (December 2007). "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". Lancet 370 (9602): 1829–39. doi:10.1016/S0140-6736(07)61778-4. PMID 18061058.
^ "Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report" (PDF). National Institutes of Health. National Heart, Lung and Blood Institute. http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf. Retrieved 2008-10-27.
^ van der Steeg WA, Holme I, Boekholdt SM, Larsen ML, Lindahl C, Stroes ES, Tikkanen MJ, Wareham NJ, Faergeman O, Olsson AG, Pedersen TR, Khaw KT, Kastelein JJ (February 2008). "High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A-I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies". J. Am. Coll. Cardiol. 51 (6): 634–42. doi:10.1016/j.jacc.2007.09.060. PMID 18261682.
^ "How Can I Lower High Cholesterol". American Heart Association. http://www.heart.org/idc/groups/heart-public/@wcm/@hcm/documents/downloadable/ucm_300460.pdf. Retrieved 2011-04-03.
^ "Good Cholesterol Foods". Good Cholesterol Foods. http://good-cholesterol-foods.net. Retrieved 2011-04-03.
^ National Institute for Health and Clinical Excellence. Clinical guideline 67: Lipid modification. London, 2008.
^ Nicholls, S. J. (2008). "Rosuvastatin and progression of atherosclerosis". Expert Review of Cardiovascular Therapy 6 (7): 925–933. doi:10.1586/14779072.6.7.925. PMID 18666843. http://www.medscape.com/viewarticle/578689. edit
^ Heart Protection Study Collaborative Group (July 2002). "MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial". Lancet 360 (9326): 7–22. doi:10.1016/S0140-6736(02)09327-3. PMID 12114036.
^ Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, MacFarlane PW, McKillop JH, Packard CJ (November 1995). "Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group". N. Engl. J. Med. 333 (20): 1301–7. doi:10.1056/NEJM199511163332001. PMID 7566020.
^ Grundy SM (May 2007). "Should women be offered cholesterol lowering drugs to prevent cardiovascular disease? Yes". BMJ 334 (7601): 982–982. doi:10.1136/bmj.39202.399942.AD. PMC 1867899. PMID 17494017. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1867899.
^ Kendrick M (May 2007). "Should women be offered cholesterol lowering drugs to prevent cardiovascular disease? No". BMJ 334 (7601): 983–983. doi:10.1136/bmj.39202.397488.AD. PMC 1867901. PMID 17494018. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1867901.
^ , (January 1988). "Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel". Arch. Intern. Med. 148 (1): 36–69. doi:10.1001/archinte.148.1.36. PMID 3422148.
^ "Cholesterol". American Heart Association. 2008-11-17. http://www.americanheart.org/cholesterol/about.jsp. Retrieved 2009-02-21.
^ "About cholesterol" – American Heart Association
^ Warnick GR, Knopp RH, Fitzpatrick V, Branson L (January 1990). "Estimating low-density lipoprotein cholesterol by the Friedewald equation is adequate for classifying patients on the basis of nationally recommended cutpoints". Clin. Chem. 36 (1): 15–9. PMID 2297909.
^ Wang, T. Y.; Newby, L. K.; Chen, A. Y.; Mulgund, J.; Roe, M. T.; Sonel, A. F.; Bhatt, D. L.; Delong, E. R. et al (2009). "Hypercholesterolemia paradox in relation to mortality in acute coronary syndrome". Clinical Cardiology 32 (9): E22–E28. doi:10.1002/clc.20518. PMID 19645040. edit
^ Anderson KM, Castelli WP, Levy D (April 1987). "Cholesterol and mortality. 30 years of follow-up from the Framingham study". JAMA 257 (16): 2176–80. doi:10.1001/jama.257.16.2176. PMID 3560398.
^ Ulmer H, Kelleher C, Diem G, Concin H (2004). "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". J Women's Health (Larchmt) 13 (1): 41–53. doi:10.1089/154099904322836447. PMID 15006277.
^ Daniel Steinberg (2007). The Cholesterol Wars: The Cholesterol Skeptics vs the Preponderance of Evidence. Boston: Academic Press. ISBN 0-12-373979-9.
^ Uffe Ravnskov (2000). The Cholesterol Myths : Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease. New Trends Publishing, Incorporated. ISBN 0-96708-970-0.
^ "How To Get Your Cholesterol Tested". American Heart Association. http://www.americanheart.org/presenter.jhtml?identifier=541. Retrieved 2009-02-21.
^ The interactive pathway map can be edited at WikiPathways: "Statin_Pathway_WP430". http://www.wikipathways.org/index.php/Pathway:WP430.

External links

Cholesterol bound to proteins in the PDB
Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults US National Institutes of Health Adult Treatment Panel III
Aspects of fat digestion and metabolism – UN/WHO Report 1994
American Heart Association – "About Cholesterol"

UpToDate Contents

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1. 一次予防における脂質（高コレステロール血症を含む）の治療 treatment of lipids including hypercholesterolemia in primary prevention
2. 血中脂質およびリポ蛋白の測定 measurement of blood lipids and lipoproteins
3. 脂質疾患に対するスクリーニング screening for lipid disorders
4. 二次予防における脂質（高コレステロール血症を含む）の治療 treatment of lipids including hypercholesterolemia in secondary prevention
5. リポ蛋白の分類、代謝、およびアテローム性動脈硬化症における役割 lipoprotein classification metabolism and role in atherosclerosis

English Journal

Effects of Encapsulated Propolis on Blood Glycemic Control, Lipid Metabolism, and Insulin Resistance in Type 2 Diabetes Mellitus Rats.

Li Y, Chen M, Xuan H, Hu F.SourceCollege of Animal Science, Zhejiang University, No. 268 Kaixuan Road, Hangzhou 310029, China.
Evidence-based complementary and alternative medicine : eCAM.Evid Based Complement Alternat Med.2012;2012:981896. Epub 2011 Jun 12.
The present study investigates the encapsulated propolis on blood glycemic control, lipid metabolism, and insulin resistance in type 2 diabetes mellitus (T2DM) rats. The animal characteristics and biological assays of body weight, fasting blood glucose (FBG), fasting serum insulin (FINS), insulin ac
PMID 21716678

High serum fasting peptide YY (3-36) is associated with obesity-associated insulin resistance and type 2 diabetes.

Ukkola OH, Puurunen VP, Piira OP, Niva JT, Lepojarvi ES, Tulppo MP, Huikuri HV.SourceInstitute of Clinical Medicine, Department of Internal Medicine, Finland; Biocenter Oulu, University of Oulu and Clinical Research Center of Oulu University Hospital, Finland.
Regulatory peptides.Regul Pept.2011 Oct 10;170(1-3):38-42. Epub 2011 May 31.
We studied whether serum fasting levels of active form of peptide YY (PYY), PYY(3-36), are associated with obesity and related phenotypes. The study population consisted of 428 patients with coronary artery disease and diagnosed type 2 diabetes and 440 patients with coronary artery disease but witho
PMID 21635925

Japanese Journal

若年発症2型糖尿病の疫学・成因・病態・治療・合併症

内潟安子
東京女子医科大学雑誌 81(E2), E154-E161, 2011-03-31
若い年齢で発症する糖尿病として1型糖尿病が有名であるが、2型糖尿病もある。30歳未満で診断された2型糖尿病を若年発症2型糖尿病として、若年発症2型糖尿病が大人発症2型糖尿病と異なる点、同年代で発症した1型糖尿病と異なる点を中心に、その全体像を明らかにする。,まず患者数は診断時年齢と病型によって異なる。10歳未満で診断される患者はほとんど1型糖尿病であり2型はわずかである。しかし、10歳代になると1 …
NAID 110008441461

ラットの血清および肝臓脂質レベルに対する食餌アマランサスの作用

川崎雅志,岡村有華,菊池美沙,新田未和,山崎真奈
岩手県立大学盛岡短期大学部研究論集 13, 51-56, 2011-03
… The effects of dietary amaranth, Amaranthus hypochondriacus, ingestion on serum and liver lipid levels were studied in rats. … Serum total cholesterol and high-density lipoprotein-cholesterol concentrations in the groups fed amaranth and amaranth-supplemented rice diets tended to increase. …
NAID 110008425676

「cholesterol」

Cholesterol
	IUPAC name (3β)-cholest-5-en-3-ol
	Other names (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
Identifiers
CAS number	57-88-5
PubChem	5997
ChemSpider	5775
UNII	97C5T2UQ7J
KEGG	D00040
ChEBI	CHEBI:16113
ChEMBL	CHEMBL112570
Jmol-3D images	Image 1
	SMILES C[C@H](CCCC(C)C)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2CC=C4[C@@]3(CC[C@@H](C4)O)C)C ;
	InChI InChI=1S/C27H46O/c1-18(2)7-6-8-19(3)23-11-12-24-22-10-9-20-17-21(28)13-15-26(20,4)25(22)14-16-27(23,24)5/h9,18-19,21-25,28H,6-8,10-17H2,1-5H3/t19-,21+,22+,23-,24+,25+,26+,27-/m1/s1 ; Key: HVYWMOMLDIMFJA-DPAQBDIFSA-N InChI=1/C27H46O/c1-18(2)7-6-8-19(3)23-11-12-24-22-10-9-20-17-21(28)13-15-26(20,4)25(22)14-16-27(23,24)5/h9,18-19,21-25,28H,6-8,10-17H2,1-5H3/t19-,21+,22+,23-,24+,25+,26+,27-/m1/s1; Key: HVYWMOMLDIMFJA-DPAQBDIFBB ;
Properties
Molecular formula	C27H46O
Molar mass	386.65 g/mol
Appearance	white crystalline powder
Density	1.052 g/cm3
Melting point	148–150 °C
Boiling point	360 °C (decomposes)
Solubility in water	0.095 mg/L (30 °C)
Solubility	soluble in acetone, benzene, chloroform, ethanol, ether, hexane, isopropyl myristate, methanol
	(verify) (what is: /?); Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
	Infobox references

　　[★] コレステロール　　

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[isbn0-12-373979-9-59] Daniel Steinberg (2007). The Cholesterol Wars: The Cholesterol Skeptics vs the Preponderance of Evidence. Boston: Academic Press. ISBN 0-12-373979-9.

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serum cholesterol