Cholesterol (from Ancient Greek chole - (bile) and stereo (solid), followed by chemical suffix -ol for alcohol) is an organic molecule. These are sterols (or steroid modifications), a type of lipid molecule, and are synthesized by all animal cells, because they are important structural components of all animal cell membranes and are essential for maintaining the integrity and fluidity of the membrane structure. Cholesterol allows animal cells to function without cell walls (which in other species protect membrane integrity and cell viability); this allows the animal cells to change shape quickly.
In addition to its importance to the structure of animal cells, cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acids and vitamin D. Cholesterol is the main sterol that is synthesized by all animals. In vertebrates, liver cells usually produce the largest amount. None between prokaryotes (bacteria and archaea), although there are some exceptions, such as Mycoplasma , which require cholesterol for growth.
FranÃÆ'§ois Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it was not until 1815 that Michel Eugène chemist Chevreul called cholesterine.
Video Cholesterol
Physiology
Since cholesterol is very important for all animal life, each cell is able to synthesize it through a complicated 37 step process, starting with the mevalonate pathway and ending up with the conversion of lanosterol to stepping 19 steps into cholesterol. Furthermore, it can be absorbed directly from animal foods.
A male man weighing 68 kg (150 lb) typically synthesizes about 1 gram (1,000 mg) per day, and his body contains about 35 g, mostly contained in cell membranes. Typical daily dietary intake of cholesterol for a man in the United States is 307 mg.
Most cholesterol is ingested in esterification, and the esterified cholesterol is poorly absorbed. The body also compensates for the absorption of extra cholesterol by reducing cholesterol synthesis. For this reason, cholesterol in the diet, seven to ten hours after consumption, has little, if any effect on the concentration of cholesterol in the blood. However, during the first seven hours after consumption of cholesterol, because the absorbed fat is distributed around the body in extracellular water by various lipoproteins (which carry all the fat in the water outside the cell), the concentration increases. It is also important to recognize, however, that the concentration measured in blood plasma samples varies with the measurement method used. Traditional, cheaper methods do not reflect (a) which lipoproteins transport various fat molecules, or (b) which cells digest, burn or export fatty molecules as a total sample of blood plasma.
Cholesterol is recycled in the body. The liver releases it in un-esterified form (through bile) into the gastrointestinal tract. Usually, about 95% of the excreted cholesterol is reabsorbed by the small intestine back into the bloodstream.
Plants make cholesterol in very small amounts. Plants produce phytosterols (chemicals similar to cholesterol), which can compete with cholesterol for reabsorption in the intestinal tract, thereby potentially lowering cholesterol reabsorption. When the lining of the intestine absorbs phytosterols, in place of cholesterol, they usually secrete the phytosterol molecules back into the gastrointestinal tract, an important protective mechanism. The natural intake of phytosterols, which include sterols and stanols, ranges from ~ 200-300 mg/day depending on eating habits. A specially designed vegetarian experimental diet has been produced producing more than 700 mg/day.
Function
Cholesterol, given that it forms about 30% of all animal cell membranes, is necessary to build and maintain the membrane and modulate membrane fluidity over the physiological temperature range. The hydroxyl group on cholesterol interacts with the polar head of the phospholipids and membrane sphingolipids, while the large steroids and hydrocarbon chains are embedded in the membrane, alongside the nonpolar fatty acid chain of the other lipids. Through interaction with the fatty acid chain of phospholipids, cholesterol increases the packing of the membranes, both of which alter membrane fluidity and maintain membrane integrity so that animal cells do not need to build cell walls (like plants and most bacteria). The membrane remains stable and durable without stiffness, allowing animal cells to change shapes and animals to move.
The tetracyclic ring structure of cholesterol contributes to the fluidity of the cell membrane, because this molecule in a conformation trans makes all but the side chains of rigid and planar cholesterol. In this structural role, cholesterol also reduces the permeability of the plasma membrane into neutral solutes, hydrogen ions, and sodium ions.
Inside the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of caved cavities and clathrin-coated holes, including cavity-dependent and clathrin-dependent endocytosis. The role of cholesterol in this type of endocytosis can be investigated using methyl beta cyclodextrin (M? CD) to remove cholesterol from the plasma membrane. Recent studies have shown that cholesterol is also involved in cell signaling processes, aiding the formation of lipid rafts in the plasma membrane, which carry receptor proteins at close range with high concentrations of second messenger molecules. In some layers, cholesterol and phospholipids, both electrical insulators, can facilitate the speed of transmission of electrical impulses along the neural network. For many neuron fibers, the myelin sheath, rich in cholesterol because it comes from a compacted layer of Schwann cell membrane, provides insulation for more efficient impulse conduction. Demielination (loss of some Schwann cells) is believed to be part of the basis for multiple sclerosis.
In cells, cholesterol is also a precursor molecule for some biochemical pathways. For example, it is a precursor molecule for the synthesis of vitamin D and all steroid hormones, including adrenal hormones adrenal cortisol and aldosterone, as well as sex hormones progesterone, estrogen, and testosterone, and its derivatives.
The liver secretes cholesterol into bile, which is then deposited in the gallbladder. Bile contains bile salts, which dissolves fat in the gastrointestinal tract and helps in the absorption of the intestines from fat molecules as well as fat-soluble vitamins, A, D, E, and K.
Biosynthesis
All animal cells produce cholesterol, both for membrane structure and other uses, with varying levels of production by cell type and organ function. About 80% of total daily cholesterol production occurs in the liver; other sites with higher levels of synthesis include the intestines, adrenal glands, and reproductive organs.
Synthesis in the body begins with a mevalonate pathway where two acetyl CoA molecules condense to form acetoacetyl-CoA. This is followed by a second condensation between acetyl CoA and acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA).
This molecule is then reduced to mevalonate by the HMG-CoA reductase enzyme. Production of mevalonate is a step that limits the rate and can not be changed in cholesterol synthesis and is the workplace for statins (cholesterol-lowering class).
Mevalonate was eventually converted to isopentenyl pyrophosphate (IPP) via two phosphorylated steps and one decarboxylation step requiring ATP.
Three molecules of isopentenyl pyrophosphate condense to form farnesyl pyrophosphate through the action of geranyl transferase.
Two farnesyl pyrophosphate molecules then condense to form squalene by the action of squalene synthase in the endoplasmic reticulum.
Oxidosqualene cyclase then cyclores the cyclase to form lanosterol. Finally, lanosterol is converted to cholesterol through a 19-step process.
The last 19 steps for cholesterol contain NADPH and Oxygen to help oxidize methyl groups to remove carbon, mutase to transfer alkene groups, and NADH to help reduce ketones.
Konrad Bloch and Feodor Lynen shared the Nobel Prize in Physiology or Medicine in 1964 for their discovery of several mechanisms and methods of regulating cholesterol and fatty acid metabolism.
Regulation of cholesterol synthesis
Cholesterol biosynthesis is directly regulated by cholesterol levels, although the homeostatic mechanism involved is only partially understood. Higher food intake causes a net decrease in endogenous production, whereas a lower intake of food has the opposite effect. The primary regulatory mechanism is the sensing of intracellular cholesterol in the endoplasmic reticulum by the SREBP protein (regulatory element-binding protein sterols 1 and 2). In the presence of cholesterol, SREBP is bound to two other proteins: SCAP (SREBP cleavage-activating protein) and INSIG-1. When cholesterol levels fall, INSIG-1 dissociates from the SREBP-SCAP complex, allowing the complex to migrate to the Golgi apparatus. Here SREBP is broken down by S1P and S2P (site protease-1 and site protease-2), 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 low-density lipoprotein (LDL) receptors and HMG-CoA reductase. LDL receptors scavenge the circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to increased production of endogenous cholesterol. Most of these signaling pathways were 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 work further demonstrates how the SREBP pathway regulates the expression of many genes that control the formation of lipids and metabolism and the fuel allocation of the body.
Cholesterol synthesis can also be switched off when cholesterol levels are high. HMG-CoA reductase contains the cytosolic domain (responsible for its catalytic function) and the membrane domain. Domain membrane senses signals for degradation. Increased concentrations of cholesterol (and other sterols) cause changes in the oligomerization state of this domain, which makes it more susceptible to damage by proteosomes. This enzyme activity can also be reduced by phosphorylation by an AMP-activated protein kinase. Since this kinase is activated by AMP, which is generated when ATP is hydrolyzed, cholesterol synthesis is stopped when ATP levels are low.
Food source
Animal fats are a complex mix of triglycerides (stored energy, see: "Introduction to Energy Storage". Ã, ), with fewer amounts of both phospholipids and cholesterol molecules from which all animal membranes (and humans) are constructed. Since all animal cells produce cholesterol, all animal-based foods contain cholesterol in varying amounts. The main sources of cholesterol diet include cheese, egg yolks, beef, pork, poultry, fish, and shrimp. Breast milk also contains a lot of cholesterol.
From a dietary point of view, plant cells do not produce cholesterol, and are not found in plant foods. Some plant foods, such as avocados, flaxseed and peanuts, contain phytosterols, which compete with cholesterol for absorption in the intestines, reducing the absorption of good cholesterol diet and bile. However, a typical diet contributes to a sequence of 0.2 grams of phytosterol, which is not enough to have a significant impact on cholesterol absorption. Feedosterol intake can be added through the use of functional foods containing phytosterols or dietary supplements that are recognized to have the potential to lower LDL-cholesterol levels. Several additional guidelines have recommended doses of phytosterols in the range of 1.6 to 3.0 grams per day (Canadian Health, EFSA, ATP III, FDA). A recent meta-analysis showed a 12% decrease in LDL-cholesterol at an average dose of 2.1 grams per day. However, the benefits of a diet supplemented with phytosterols have been questioned.
By 2016, the United States Department of Agriculture's Diet Guidance Advisory Committee recommends that Americans eat as little cholesterol food as possible. Increased food intake from industrial trans fats is associated with an increased risk in all causes of death and cardiovascular disease. Trans fats have been shown to reduce HDL levels while increasing LDL levels. Based on evidence and evidence that involves low HDL and high LDL levels in cardiovascular disease (see Hypercholesterolemia), many health authorities recommend reducing LDL-cholesterol through dietary changes other than other lifestyle modifications. Mice with high-fat or fructose diets become dyslipidemic. However, a well-controlled randomized controlled trial that investigates patient-related results from a low-fat diet for healthy people with poor hypercholesterolaemia. In addition, for familial hypercholesterolemia, large, parallel, controlled randomized trials are still needed to investigate the effectiveness of cholesterol-lowering diet and the addition of omega-3 fatty acids, soy protein, sterols or stanols.
Plasma transport and absorption settings
As an isolated molecule, cholesterol is only slightly soluble in water; it dissolves into the bloodstream (water based) only at very small concentrations. In contrast, cholesterol is transported in lipoproteins, complex discoid particles with exterior and lipid amphiphilic proteins, surface-facing outward water-soluble and surface-facing fat-soluble surfaces; ie transport through emulsification. Triglycerides and cholesterol esters are carried out internally. Phospholipids and cholesterol, the amphipathic, are transported on the monolayer surface of the lipoprotein particles.
There are several types of lipoproteins in the blood. In order to increase their density, they are kilomikron, very low density lipoprotein (VLDL), medium density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Lower protein/lipid ratios produce less dense lipoproteins. Cholesterol in different lipoproteins is identical, although some are carried as genuine "free" alcoholic forms (OH-cholesterol groups face the water surrounding the particles), while others as acyl fatty esters, also known as cholesterol esters, in particles.
The lipoprotein particles are organized by the apolipoprotein complex, typically 80-100 different proteins per particle, which can be recognized and bound by specific receptors on the cell membrane, directing their lipid load into the cell and the specific tissue that is currently ingesting the fat transporting particles. The lipoprotein particles thus include molecular addresses that play a key role in the distribution and delivery of fat around the body in the water outside the cell.
Chylomicrons, the most dense cholesterol transport molecule, contain apolipoprotein B-48, apolipoprotein C, and apolipoprotein E (the main cholesterol carrier in the brain) in its shell. Chylomicrons carry fat from the intestines to muscles and other tissues that require fatty acids for energy or fat production. Unused cholesterol still remains in the chylomicron remnants that are rich in cholesterol, and are taken from here to the bloodstream by the liver.
The VLDL molecule is produced by the liver of triacylglycerol and cholesterol not used in bile acid synthesis. These molecules contain apolipoprotein B100 and apolipoprotein E in their shells, and are degraded by lipoprotein lipase in blood vessel walls to IDL.
Blood vessels divide and absorb triacylglycerol from IDL molecules, increasing cholesterol concentration. The IDL molecule is then consumed in two processes: half metabolized by HTGL and taken by LDL receptors on the liver cell surface, while the other half continues to lose triacylglycerol in the bloodstream until they become LDL molecules, with the highest concentration of cholesterol. inside it.
LDL particles are the main blood cholesterol carriers. Each contains about 1,500 cholesterol ester molecules. The molecule of LDL molecule contains only one B100 apolipoprotein molecule, which is recognized by LDL receptors in peripheral tissues. After binding of apolipoprotein B100, many LDL receptors concentrate in clathrin-coated holes. Both LDL and its receptors form vesicles in cells through endocytosis. The vesicles then fuse with lysosomes, where the liposic acid lipase enzyme hydrolyzes the cholesterol ester. Cholesterol can then be used for membrane biosynthesis or esterified and stored in the cell, so as not to disrupt the cell membrane.
The LDL receptor is used during cholesterol absorption, and the synthesis is regulated by SREBP, the same protein that controls the synthesis of cholesterol de novo , according to its presence in the cell. Cells with abundant cholesterol will have synthesis of blocked LDL receptors, to prevent new cholesterol in LDL molecules taken. In contrast, LDL receptor synthesis occurs when cells are deprived of cholesterol.
When this process becomes irregular, LDL molecules without receptors begin to appear in the blood. These LDL molecules are oxidized and taken up by macrophages, which become enlarged and form foam cells. These foam cells are often trapped in blood vessel walls and contribute to the formation of atherosclerotic plaques. Differences in cholesterol homeostasis affect the development of early atherosclerosis (carotid intima-media thickness). This plaque is a major cause of heart attacks, strokes, and other serious medical problems, leading to an association called LDL cholesterol (actually lipoproteins) with "bad" cholesterol.
HDL particles are thought to transport cholesterol back to the liver, either for excretion or for other hormone synthesizing tissues, in a process known as RCC transport. A large number of HDL particles are correlated with better health outcomes, whereas low numbers of HDL particles are associated with the development of atheromatous disease in the arteries. Metabolism, recycling, and excretion
Cholesterol is susceptible to oxidation and easily forms an oxygen derivative known as oxysterols. Three different mechanisms can form this: autoxidation, secondary oxidation to lipid peroxidation, and oxidation of cholesterol enzyme enzymes. Great attention to oxysterols arises when they are shown to perform inhibitory measures on cholesterol biosynthesis. This finding came to be known as the "oxysterol hypothesis". Additional roles for oxysterols in human physiology include their participation in the biosynthesis of bile acids, serving as a form of cholesterol transport, and the regulation of gene transcription.
In biochemical experiments, dissolved forms of cholesterol, such as tritiated-cholesterol are used. This derivative is degraded in storage and is essential for purifying cholesterol before use. Cholesterol can be purified using a small Sephadex LH-20 column.
Cholesterol is oxidized by the liver to a variety of bile acids. This, in turn, is conjugated with glycine, taurine, glucuronic acid, or sulfate. The mixture of conjugated and unconjugated bile acids, along with the cholesterol itself, is removed from the liver into the bile. Approximately 95% of bile acids are reabsorbed from the intestine, and the remainder is lost in the stool. Excretion and reabsorption of bile acids form the basis of enterohepatic circulation, which is essential for the digestion and absorption of dietary fat. In certain circumstances, when more concentrated, such as in the gallbladder, cholesterol crystallizes and is the main constituent of most gallstones (lecithin and bilirubin gallstones also occur, but more rarely). Every day, up to 1 g of cholesterol enters the colon. This cholesterol comes from diet, bile, and damaged intestinal cells, and can be metabolized by colonic bacteria. Cholesterol is converted primarily into coprostanol, an unabsorbed sterol that is excreted in the feces. The origin of cholesterol-lowering bacteria has been isolated from human waste.
Although cholesterol is a steroid commonly associated with mammals, the human pathogen Mycobacterium tuberculosis is able to completely decompose this molecule and contain a large number of genes regulated by its presence. Many of these cholesterol-regulated genes are homologous fatty acid-oxidation genes, but have evolved in such a way as to bind to large steroid substrates such as cholesterol.
Research
Cholesterol binds and affects the gating of a number of ion channels such as nicotinic acetylcholine receptors, GABA receptors A , and potassium receptor ion channels into. Cholesterol also activates alpha estrogen-related receptors (ERR?), And may be endogenous ligands for receptors. The constitutive nature of receptors can be explained by the fact that cholesterol is ubiquitous in the body. ERR Inhibition? signals with reduced cholesterol production have been identified as a key mediator of statin and bisphosphonate effects on bone, muscle, and macrophages. On the basis of these findings, have suggested that ERR? should be de-orphanized and classified as receptors for cholesterol.
Maps Cholesterol
Clinical interests
Hypercholesterolemia
According to the lipid hypothesis, since cholesterol (like all fat molecules) is transported around the body (in the water outside the cells) within the lipoprotein particles, high cholesterol concentrations (hypercholesterolaemia) potentially offer a lower cost way to estimate LDL particle concentration; Perhaps even low concentrations of HDL functional particles, both variations are strongly associated with cardiovascular disease because LDL particles promote the development of atheromas in the arteries (atherosclerosis).
This process of atherosclerotic disease, for decades, causes myocardial infarction (heart attack), stroke, and peripheral vascular disease. Because higher blood LDL, especially higher concentrations of LDL particles and smaller LDL particle size, contribute to this process more than cholesterol levels from HDL particles, LDL particles are often called "bad cholesterol" because they have been associated with the formation of atheromas. 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". This balance is largely determined genetically, but can be changed by body builds, medications, food choices, and other factors.
Conditions with high concentrations of oxidized LDL particles, especially small solid LDL particles (sdLDL), are associated with the formation of atheromas in the artery walls, a condition known as atherosclerosis, which is a major cause of coronary heart disease and other forms of cardiovascular disease. In contrast, HDL particles (especially large HDL) have been identified as a mechanism in which cholesterol and inflammatory mediators can be excreted from atheromas. Increased HDL concentrations correlated with lower rates of atheroma progression and even regression. A 2007 study collecting data on nearly 900,000 subjects in 61 cohorts showed that total blood cholesterol levels had an exponential effect on total and cardiovascular death, with associations more prominent in younger subjects. However, since cardiovascular disease is relatively rare in younger populations, the effects of high cholesterol on health are still greater in older people.
Increased lipoprotein, LDL, IDL and VLDL fractions are considered atherogenic (susceptible to atherosclerosis). The rate of this fraction, rather than total cholesterol, correlates with the rate and progress of atherosclerosis. In contrast, total cholesterol can be within normal limits, but mainly consist of small LDL and small HDL particles, where the condition of atheroma growth rate will remain high. Recently, post hoc analysis of IDEAL and EPIC prospective studies found an association between high HDL cholesterol levels (adjusted for both apolipoprotein AI and apolipoprotein B) and an increased risk of cardiovascular disease, raising doubts about the role of cardioprotective " good cholesterol ".
Increased cholesterol levels are treated with a strict diet consisting of low saturated fat, fat-free trans, low cholesterol foods, often followed by one of a variety of hypolipidemic agents, such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants. The previous extreme cases have been dealt with partial ileal bypass surgery, which has now been replaced by drugs. Apheresis-based treatments are still used for very severe hyperlipemia that is unresponsive to treatment or requires rapid reduction of blood lipids. There are several international guidelines on the treatment of hypercholesterolaemia.
Some human trials using HMG-CoA reductase inhibitors, known as statins, have repeatedly asserted that changing the lipoprotein transport pattern from unhealthy to healthy patterns significantly decreases the incidence of cardiovascular disease, even for people with low cholesterol values ​​currently considered adults. The study also found that statins reduce the development of atheromas. As a result, people with a history of cardiovascular disease may benefit from statins regardless of their cholesterol levels (total cholesterol below 5.0 mmol/L [193 mg/dL]), and in men without cardiovascular disease, there is a benefit of lowering high cholesterol which is not normal ("primary prevention"). Primary prevention in women was initially performed only by extension of the findings in the study in men, because, in women, no large statin test performed before 2007 showed a statistically significant decrease in overall mortality or at cardiovascular end points. In 2008, a large clinical trial reported that, in seemingly healthy adults with elevated levels of inflammatory biomarkers, high sensitivity of C-reactive protein but with low baseline LDL, 20 mg/day of rosuvastatin for 1.9 years resulted in a 44% in cardiovascular events and 20% reduction in all causes of death; the effect is statistically significant for both sexes. Although these results met with some skepticism, then the study and meta-analysis also showed a statistically significant (but smaller) decrease in all cardiovascular causes and deaths, with no significant heterogeneity by sex.
The 1987 National Cholesterol Education Program report, Adult Care Panel shows that total blood cholesterol levels should: & lt; 200 mg/dL normal blood cholesterol, 200-239 mg/dL upper limit, & gt; 240 mg/dL high cholesterol. The American Heart Association provides a set of similar guidelines for total (fasting) blood cholesterol levels and heart disease risk:
However, since current testing methods determine LDL ("bad") and HDL ("good") cholesterol separately, this simple outlook becomes somewhat outdated. The desired LDL level is considered to be less than 130 mg/dL (2.6 mmol/L), although a newer upper limit of 70 mg/dL (1.8 mmol/L) may be considered in high-risk individuals based on multiple trials mentioned above. A ratio of total cholesterol to HDL - another useful measure - far less than 5: 1 is considered healthier.
Total cholesterol is defined as the amount of HDL, LDL, and VLDL. Typically, only total, HDL, and triglycerides are measured. For cost reasons, VLDL is usually estimated to be one fifth of triglycerides and LDL is estimated using the Friedewald (or variant) formula: approximate LDL = [total cholesterol] - [total HDL] - [estimated VLDL]. VLDL can be calculated by dividing total triglycerides by five. Direct LDL measurements are used when triglycerides exceed 400 mg/dL. It is estimated that VLDL and LDL have more errors when the triglycerides are above 400 mg/dL.
Given the well-known role of cholesterol in cardiovascular disease, several studies have shown an inverse correlation between cholesterol and mortality. A 2009 study of patients with acute coronary syndromes found a correlation of hypercholesterolaemia with better death outcomes. In the Framingham Heart Study, in subjects over 50, they found an 11% increase overall and a 14% increase in cardiovascular disease mortality per 1 mg/dL per year of total cholesterol reduction. The researchers attribute this phenomenon to the fact that people with severe chronic disease or cancer tend to have lower cholesterol levels than normal. This explanation is not supported by the Vorarlberg Health Monitoring and Promotion Program, where men of all ages and women over 50 years with very low cholesterol are likely to die of cancer, liver disease, and mental illness. These results indicate the effects of low cholesterol occur even among younger respondents, contrary to previous assessments among cohorts of older people that this is a proxy or a marker for the fragility that occurs with age.
Although most doctors and medical scientists consider that there is a relationship between cholesterol and atherosclerosis as discussed above, the 2014 meta-analysis of more than 500,000 patients concluded that there was insufficient evidence to support the recommendation of high consumption of polyunsaturated and low fatty acids. total saturated fat consumption for cardiovascular health.
Hypocholesterolemia
Very low cholesterol levels are called hypocholesterolemia . Research on the cause of this condition is relatively limited, but several studies have shown a link to depression, cancer, and cerebral hemorrhage. In general, low cholesterol levels seem to be a consequence, not a cause, an underlying disease. Genetic defects in cholesterol synthesis cause Smith-Lemli-Opitz syndrome, which is often associated with low plasma cholesterol levels. Hyperthyroidism, or other endocrine disorders that cause increased regulation of LDL receptors, may lead to hypocholesterolemia.
Cholesterol Test
The American Heart Association recommends testing cholesterol every 4-6 years for people aged 20 and over. A separate set of American Heart Association guidelines issued in 2013 showed that patients taking statin drugs should have their cholesterol tested 4-12 weeks after their first dose and then every 3-12 months thereafter.
Blood samples after 12 hours of fasting were taken by the doctor, or a home cholesterol monitoring tool used to determine the lipoprotein profile. It measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol, and triglycerides. It is advisable to test cholesterol at least every five years if a person has a total cholesterol of 5.2 mmol/L or more (200 mg/dL), or if a man over the age of 45 or a woman over the age of 50 has HDL (good) cholesterol from 1 mmol/L (40 mg/dL), or there are other risk factors for heart disease and stroke. Other risk factors for heart disease include Diabetes, Hypertension (or use of anti-hypertensive medications), low HDL, family history of CAD and hypercholesterolemia, and smoking.
Interactive path map
Click on the genes, proteins and metabolites below to link to each article.
Colonic liquid crystals
Some cholesterol derivatives (among other simpler cholesteric lipids) are known to produce "liquid cholesteric phase" crystals. The cholesteric phase is, in fact, the chiral nematic phase, and it changes color when the temperature changes. This makes cholesterol derivatives useful to show the temperature in liquid crystal display and temperature sensitive thermometers.
Stereoisomers
Cholesterol has 256 stereoisomers emerging from its eight stereosomers, although only two stereoisomers have biochemical significance ( nat -cholesterol and ent -cholesterol, because natural and enantiomer , respectively), and only one appears naturally ( grout -cholesterol).
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Referensi
Tautan eksternal
- "Tentang kolesterol". American Heart Association. Diarsipkan dari yang asli pada 3 Oktober 2001. < rentang>
- "Memahami uji kolesterol". Lab Tes Online . American Association for Clinical Chemistry.
Source of the article : Wikipedia
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