コレステロール　　

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an animal sterol that is normally synthesized by the liver; the most abundant steroid in animal tissues (同)cholesterin

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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)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/11/06 23:05:11」(JST)

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

Cholesterol, from the Ancient Greek chole- (bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol, is an organic molecule. It is a sterol (or modified steroid),^[3] and an essential structural component of animal cell membranes that is required to establish proper membrane permeability and fluidity. Cholesterol is thus considered within the class of lipid molecules.

In addition to its importance within cells, cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acids, and vitamin D.^[4] Cholesterol is the principal sterol synthesized by animals, all cells; in vertebrates the liver typically produces greater amounts than other cells. It is almost completely absent among prokaryotes (i.e., bacteria), although there are some exceptions such as Mycoplasma, which require cholesterol for growth.^[5]

François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it was not until 1815 that chemist Michel Eugène Chevreul named the compound "cholesterine".^[6]^[7]

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 Clinical significance
- 2.1 Hypercholesterolemia
- 2.2 Hypocholesterolemia
- 2.3 Cholesterol testing
3 Interactive pathway map
4 Cholesteric liquid crystals
5 Stereoisomers
6 See also
7 Additional images
8 References
9 External links

Physiology[edit]

Since cholesterol is essential for all animal life, each cell synthesizes it from simpler molecules, a complex 37-step process that starts with the intracellular protein enzyme HMG-CoA reductase. However, normal and particularly high levels of fats (including cholesterol) in the blood circulation, depending on how they are transported within lipoproteins, are strongly associated with the progression of atherosclerosis.

For a man of about 68 kg (150 pounds), typical total body-cholesterol synthesis is approximately 1 g (1,000 mg) per day, and total body content is approximately 35 g, primarily located within the membranes of all the cells of the body. Typical daily dietary intake of additional cholesterol, in the United States, is 200–300 mg.^[8]

Most ingested cholesterol is esterified, and esterified cholesterol is poorly absorbed. The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis.^[9] For these reasons, cholesterol intake in food has little, if any, effect on total body cholesterol content or concentrations of cholesterol in the blood.

Cholesterol is recycled. The liver excretes it in a non-esterified form (via bile) into the digestive tract. Typically about 50% of the excreted cholesterol is reabsorbed by the small bowel back into the bloodstream.

Plants make cholesterol in very small amounts.^[10] Plants manufacture phytosterols (substances chemically similar to cholesterol produced within plants), which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption.^[11] When intestinal lining cells absorb phytosterols, in place of cholesterol, they usually excrete the phytosterol molecules back into the GI tract, an important protective mechanism.

Function[edit]

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.^[12] The structure of the tetracyclic ring of cholesterol contributes to the decreased fluidity of the cell membrane as the molecule is in a trans conformation making all but the side chain of cholesterol rigid and planar.^[13] In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes,^[14] protons, (positive hydrogen ions) and sodium ions.^[15]

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.^[16] 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.^[17]

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.^[4]

Some research indicates cholesterol may act as an antioxidant.^[18]

Dietary sources[edit]

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.^[19] Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, fish, and shrimp.^[20] Human breast milk also contains significant quantities of cholesterol.^[21]

From a dietary perspective, cholesterol is not found in significant amounts in plant sources.^[20]^[22] 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.^[23] 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.^[24] 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.^[25] However, the benefits of a diet supplemented with phytosterol has been questioned.^[26]^[27]

Fat intake also plays a role in blood-cholesterol levels. This effect is thought^{[by whom?]} to come about by changes in the quantity of cholesterol and lipoproteins that are synthesized by the body. Isocalorically replacing dietary carbohydrates with monounsaturated and polyunsaturated fats has been shown to lower serum LDL and total cholesterol levels and increase serum HDL levels, while replacing carbohydrates with saturated fat was shown to increase HDL, LDL, and total cholesterol levels.^[28] Trans fats have been shown to reduce levels of HDL while increasing levels of LDL.^[29] 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.^[30] 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.^[31] 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.^[32] Other research has found that an increase in the consumption of saturated fats and cholesterol decreases overall serum cholesterol.^[33]

Biosynthesis[edit]

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).^[34] This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. This 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.^[34] Oxidosqualene cyclase then cyclizes squalene to form lanosterol. Finally, lanosterol is converted to cholesterol through a 19-step process.^[35]^[36]

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[edit]

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).^[37] 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, which allows the complex to migrate to the Golgi apparatus. Here 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 LDL receptor former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol.^[38] 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 also be turned off when cholesterol levels are high. HMG-CoA reductase contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain. The membrane domain senses 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.^[39]

Plasma transport and regulation of absorption[edit]

Metabolism, recycling and excretion[edit]

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.^[43] 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.^[44]

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.^[45]

Cholesterol is oxidized by the liver into a variety of bile acids.^[46] 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.^[47] 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.^[48] 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.^[49]^{[non-primary source needed]}

Clinical significance[edit]

Hypercholesterolemia[edit]

Main articles: hypercholesterolemia and lipid hypothesis

According to the lipid hypothesis, abnormal cholesterol levels (hypercholesterolemia) — actually higher concentrations of LDL particles and lower concentrations of functional HDL particles — 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,^[50] 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.^[51] Resistin, a protein secreted by fat tissue, has been shown to increase the production of LDL in human liver cells and also degrades LDL receptors in the liver. As a result, the liver is less able to clear cholesterol from the bloodstream. Resistin accelerates the accumulation of LDL in arteries, increasing the risk of heart disease. Resistin also adversely impacts the effects of statins, the main cholesterol-reducing drug used in the treatment and prevention of cardiovascular disease.^[52]

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.^[53]

Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL are regarded as atherogenic (prone to cause atherosclerosis).^[54] 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. 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".^[55]

Elevated cholesterol levels are treated with a strict diet consisting of low saturated fat, trans fat-free, low cholesterol foods,^[56]^[57] often followed by one of various hypolipidemic agents, such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants.^[58] 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.^[59] As a result, people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels (total cholesterol below 5.0 mmol/L [193 mg/dL]),^[60] and in men without cardiovascular disease, there is benefit from lowering abnormally high cholesterol levels ("primary prevention").^[61] Primary prevention in women is practiced only by extension of the findings in studies on men,^[62] since in women, none of the large statin trials has shown a reduction in overall mortality or in cardiovascular endpoints.^[63]

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.^[64] The American Heart Association provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease:^[65]

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),^[66] 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.

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.^[67]

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.^[68] 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.^[69] 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.^[70]

The vast majority of doctors and medical scientists consider that there is a link between cholesterol and atherosclerosis as discussed above;^[71] a small group of scientists, united in The International Network of Cholesterol Skeptics, questions the link.^[72]

Hypocholesterolemia[edit]

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.^[53] A genetic defect in cholesterol synthesis causes Smith-Lemli-Opitz syndrome, which is often associated with low plasma cholesterol levels.

Cholesterol testing[edit]

The American Heart Association recommends testing cholesterol every five years for people aged 20 years or older.^[73]

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 5.2 mmol/L or more (200+ mg/dL), or if a man over age 45 or a woman over age 50 has HDL (good) cholesterol less than 1 mmol/L (40 mg/dL), or there are other risk factors for heart disease and stroke.

Interactive pathway map[edit]

Click on genes, proteins and metabolites below to link to respective articles. ^{[§ 1]}

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Statin Pathway edit

^ The interactive pathway map can be edited at WikiPathways: "Statin_Pathway_WP430".

Cholesteric liquid crystals[edit]

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.

Stereoisomers[edit]

Cholesterol has 256 stereoisomers, although only two of them are of biochemical significance (nat-cholesterol and ent-cholesterol^[74]^[75]), and only one of them occurs naturally (nat-cholesterol).

Additional images[edit]

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

References[edit]

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^ Javitt NB (December 1994). "Bile acid synthesis from cholesterol: regulatory and auxiliary pathways". FASEB J. 8 (15): 1308–11. PMID 8001744.
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^ Marschall HU, Einarsson C (June 2007). "Gallstone disease". J. Intern. Med. 261 (6): 529–42. doi:10.1111/j.1365-2796.2007.01783.x. PMID 17547709.
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^ "Canadian scientists discover cause of high cholesterol".
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^ "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. Retrieved 2008-10-27.
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^ "How Can I Lower High Cholesterol". American Heart Association. Retrieved 2011-04-03.
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^ "Cholesterol". American Heart Association. 17 November 2008. Retrieved 2009-02-21.
^ "About cholesterol" – American Heart Association
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^ Wang TY, Newby LK, Chen AY, Mulgund J, Roe MT, Sonel AF, Bhatt DL, DeLong ER, Ohman EM, Gibler WB, Peterson ED (September 2009). "Hypercholesterolemia paradox in relation to mortality in acute coronary syndrome". Clin Cardiol 32 (9): E22–8. doi:10.1002/clc.20518. PMID 19645040.
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^ 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 0-9670897-0-0.
^ "How To Get Your Cholesterol Tested". American Heart Association. Retrieved 2013-07-10.
^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593805/
^ http://www.ncbi.nlm.nih.gov/pubmed/22869373

External links[edit]

Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults US National Institutes of Health Adult Treatment Panel III
American Heart Association – "About Cholesterol"
Cholesterol at Lab Tests Online
Cholesterol: analyte monograph from The Association for Clinical Biochemistry and Laboratory Medicine

UpToDate Contents

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1. 高コレステロール血症の治療のためのATP IIIガイドライン atp iii guidelines for treatment of high blood cholesterol
2. 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
3. 脂質異常症に対するスクリーニングガイドライン screening guidelines for dyslipidemia
4. 小児における脂質異常症の定義およびスクリーニング definition and screening for dyslipidemia in children
5. 小児の脂質異常症ののマネージメント management of pediatric dyslipidemia

English Journal

Characterization and storage stability of astaxanthin esters, fatty acid profile and α-tocopherol of lipid extract from shrimp (L. vannamei) waste with potential applications as food ingredient.

Gómez-Estaca J1, Calvo MM2, Álvarez-Acero I3, Montero P3, Gómez-Guillén MC3.
Food chemistry.Food Chem.2017 Feb 1;216:37-44. doi: 10.1016/j.foodchem.2016.08.016. Epub 2016 Aug 8.
In this work a lipid extract from shrimp waste was obtained and characterized. The most abundant fatty acids found were C16:0, C18:2n6c, C18:1n9c, C22:6n3, and C20:5n3. The extract contained all-trans-astaxanthin, two cis-astaxanthin isomers, 5 astaxanthin monoesters, and 10 astaxanthin diesters (7�
PMID 27596389

Metabolic impact of 100% fruit juice consumption on antioxidant/oxidant status and lipid profiles of adults: An Evidence-Based review.

Crowe-White K1, Parrott JS2, Stote KS3, Gutschall M4, Benson-Davies S5, Droke E6, O'Neil CE7, Wolfram T8, Ziegler P9.
Critical reviews in food science and nutrition.Crit Rev Food Sci Nutr.2017 Jan 2;57(1):152-162.
One hundred percent fruit juice (FJ) contains bioactive compounds with antioxidant activity. As such, this fruit form has the potential to improve antioxidant status and mediate outcomes influenced by redox status. A systematic review of the literature published between 1995 and 2013 was conducted u
PMID 26596639

Enhancement of Lytic Activity by Leptin Is Independent From Lipid Rafts in Murine Primary Splenocytes.

Collin A1,2, Noacco A3,4, Talvas J3,4, Caldefie-Chézet F3,4, Vasson MP3,4,5, Farges MC3,4.
Journal of cellular physiology.J Cell Physiol.2017 Jan;232(1):101-9. doi: 10.1002/jcp.25394. Epub 2016 Apr 7.
Leptin, a pleiotropic adipokine, is known as a regulator of food intake, but it is also involved in inflammation, immunity, cell proliferation, and survival. Leptin receptor is integrated inside cholesterol-rich microdomains called lipid rafts, which, if disrupted or destroyed, could lead to a pertu
PMID 27028718

Stiffness of Intact Endothelial Cells From Fresh Aortic Bifurcations of Atherosclerotic Rabbits-Atomic Force Microscopic Study.

Hayashi K1,2, Higaki M3.
Journal of cellular physiology.J Cell Physiol.2017 Jan;232(1):7-13. doi: 10.1002/jcp.25379. Epub 2016 Aug 10.
Stiffness of intact endothelial cells (ECs) in the abdominal aorta (AA) and in the medial and lateral wall of the common iliac artery (CIA(Medial) and CIA(Lateral), respectively), which were freshly obtained from cholesterol-fed rabbits, were measured with an atomic force microscopic indentation met
PMID 26991605

Japanese Journal

コレステロール結晶塞栓症の早期診断と対策

塩見智子/木原健
東京女子医科大学雑誌 82(E2), E362-E369, 2012-07-31
… コレステロール結晶塞栓症(Cholesterol Crystal Embolization: CCE)は、大動脈壁のアテローマが崩壊、流出して生じたコレステロール結晶による全身性の塞栓症である。 …
NAID 110009435914

コレステロール結晶塞栓症の早期診断と対策

塩見智子/木原健
東京女子医科大学雑誌 82(E2), E362-E369, 2012-07-31
… コレステロール結晶塞栓症(Cholesterol Crystal Embolization: CCE)は、大動脈壁のアテローマが崩壊、流出して生じたコレステロール結晶による全身性の塞栓症である。 …
NAID 110009435896

Characteristics of Himalayan Marmots and Their Response to an Atherogenic Diet

LI Yafeng,WANG Zhongdong,TAO Yuanqing [他]
Experimental animals 61(4), 461-466, 2012-07
NAID 40019342181

Related Pictures

★リンクテーブル★

リンク元	「副腎皮質ホルモン」「コレステロール」「Chl」「Cho」
拡張検索	「cholesterol 7alpha-hydroxylase」

「副腎皮質ホルモン」

Cholesterol
	IUPAC name (3β)-cholest-5-en-3-ol
	Systematic name 2,15-dimethyl-14-(1,5-dimethylhexyl)tetracyclo[8.7.0.02,7.011,15]heptacos-7-en-5-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, Cholesterin, Cholesteryl alcohol
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
Hazards
Flash point	209.3 ±12.4°C
	(verify) (what is: /?); Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
	Infobox references

　　[★]

英: adrenocortical hormone
同: 副腎皮質ステロイド adrenocorticoids
関: 副腎皮質刺激ホルモン放出ホルモン、副腎皮質刺激ホルモン; ステロイド
関: 副腎、副腎皮質、ステロイド、コルチコステロイド、ステロイドホルモン、コルチコイド。副腎皮質ホルモン剤

図：SP.891(組織),892(構造式)
副腎皮質の球状層、索状層、網状層で合成される

種類(主要なもののみ)

電解質コルチコイド

球状層から分泌される。アルドステロン

糖質コルチコイド

索状層から分泌される。コルチゾール

副腎アンドロジェン

網状層から分泌される。アンドロステンジオン

コレステロール cholesterol
↓CYP11A1
プレグネノロン pregnenolone	－－→ CYP17 17α-hydroxylase	17α-ヒドロキシプレグネノロン 17α-hydroxypregnenolone	－－→ CYP17 17α-hydroxylase	デヒドロエピアンドロステロン dehydroepiandrosterone DHEA
↓3β-HSD 3β-hydroxysteroid dehydrogenase		↓3β-HSD		↓3β-HSD
プロゲステロン progesterone	－－→ CYP17 17α-hydroxylase	17α-ヒドロキシプロゲステロン 17α-hydroxyprogesterone	－－→ CYP17 17α-hydroxylase	アンドロステンジオン androstenedione Δ⁴androstene-3,17-dion
↓CYP21 21-hydroxylase		↓CYP21 21-hydroxylase
デオキシコルチコステロン deoxycorticosterone		11-デオキシコルチゾール 11-deoxycortisol
↓CYP11B2　11β-hydroxylase		↓CYP11B1　11β-hydroxylase
コルチコステロン corticosterone		コルチゾール cortisol
↓CYP11B2 18-hydroxylase
18-ヒドロキシコルチコステロン 18-hydroxycorticosterone
↓CYP11B2 18-hydroxydehydrogenase
アルドステロン aldosterone

球状増 zona glomerulosa		索状層 zona fasciculata		網状層 zona reticularis

臨床関連

21-hydroxylaseが正常に機能しないことにより生じる (L.320)

薬理学

副腎皮質ホルモン製剤

副腎皮質から分泌されるホルモン (SP.895)

名称		血漿濃度 (ng/ml)	1日分泌量 (mg/day)
糖質コルチコイド	コルチゾール	40～180	15～20
糖質コルチコイド	コルチコステロン	2～6	2～5
鉱質コルチコイド	アルドステロン	0.05～0.20	0.05～0.15
鉱質コルチコイド	11-DOC	0.05～0.30	0.10～0.20
副腎アンドロジェン	DHEA	2～8	7～15
	DHEA-S	1～4
	アンドロステンジオン	1～2	2～3

「コレステロール」

　　[★]

英: cholesterol
同: コレステリン cholesterin
関: lipoprotein

コレステロールは多くの場合、長鎖脂肪酸のコレステロールエステルとして食品に多く含まれる (SP.739)

分子式

C27H46O = 386.66

吸収

小腸から放出された脂質とコレステロールはアポ蛋白とカイロミクロンを形成する。
カイロミクロンは血液循環に入り、循環中にカイロミクロンレムナント chylomicron remnantとなる。

カイロミクロンに含まれる脂質は、血管内皮に存在するリポ蛋白リパーゼ(LPL)により分解されて脂肪酸を遊離し、コレステロールの比が高いカイロミクロンレムナントとなる。

肝臓はカイロミクロンレムナントを取り込む

生合成

コレステロールは酢酸を原料として合成される。

acetyl-CoA→hydroxymethyl-glutaryl coenzyme A(HMG-CoA)－(HMG-CoA reductase)→mebaronate→･･･→コレステロール

→コレステロールの生合成

体内循環

肝臓は血液循環にVLDLを放出する

血液循環中のVLDLの脂質は、、血管内皮に存在するリポ蛋白リパーゼ(LPL)により分解されて脂肪酸を遊離し、コレステロールの比が高いIDL、LDLとなる。

組織からはコレステロール比型が高いHDLが放出され、そのまま肝臓に取り込まれるか、IDLにコレステロールを渡すことでコレステロールの逆輸送を行っている(内因性の抗動脈硬化作用)。

肝臓は血液循環からHDL, IDL, VDLを受容体を介して取り込む

排泄

肝臓でコレステロールは胆汁酸に変換され、胆汁として排出される

see HBC.236

Lipoprotein	Source	Diameter (nm)	Density (g/mL)	Composition		Main Lipid Components	Apolipoproteins
				Protein	Lipid
				(%)	(%)
Chylomicrons	Intestine	90～100	< 0.95	1～2	98.99	Triacylglycerol	A-I, A-II, A-IV,1 B-48, C-I, C-II, C-III, E
Chylomicron remnants	Chylomicrons	45～150	< 1.006	6～8	92.94	Triacylglycerol, phospholipids, cholesterol	B-48, E
VLDL	Liver (intestine)	30～90	0.95～1.006	7～10	90～93	Triacylglycerol	B-100, C-I, C-II, C-III
IDL	VLDL	25～35	1.006～1.019	11	89	Triacylglycerol, cholesterol	B-100, E
LDL	VLDL	20～25	1.019～1.063	21	79	Cholesterol	B-100
HDL1	Liver, intestine, VLDL, chylomicrons	20～25	1.019.1.063	32	68	Phospholipids, cholesterol	A-I, A-II, A-IV, C-I, C-II, C-III, D,2 E
HDL2		10～20	1.063～1.125	33	67
HDL3		5～10	1.125～1.210	57	43
Preβ-HDL3		< 5	> 1.210				A-I
Albumin/free fatty	Adipose acids tissue		> 1.281	99	1	Free fatty acids

基準値

総コレステロール　：＜220 mg/dl
HDLコレステロール：≧40 mg/dl
LDLコレステロール：＜140 mg/dl

脂質異常症→　血清：Total-CHO≧220 mg/dl。LDL-C≧140 mg/dl。TG≧150 mg/dl。HDL-C＜40 mg/dl

参考

1.

http://rockymuku.sakura.ne.jp/naibunnpitunaika/koresutero-runotanninokannzann.pdf

「Chl」

　　[★] コレステロール cholesterol

「Cho」