Cholesterol Essay

Dyslipidemia is characterized by increased total cholesterol levels, low-density lipoprotein-cholesterol levels (LDL-C), triglyceride levels (TG), and low high-density lipoprotein-cholesterol levels (HDL-C) (1). Most of the cholesterols in the body (60-70%) are transported to liver cells in the form of LDL-C through direct interaction with specific LDL receptors (1). Dietary intake of foods that are high in cholesterol and saturated fats (such as egg yolk, butter, fast food) activates a feedback mechanism which lowers the activity of LDL receptors. As a consequence, LDLs are no longer being efficiency recycled to the liver and plasma LDL levels increased dramatically (1). The excess circulating LDLs are able to migrate through endothelial

Our body naturally produces cholesterol through the liver, we can also obtain cholesterol from consumed products. We need small amounts of cholesterol to produce hormones, bile, and vitamin D. Cholesterol doesn’t dissolve in the bloodstream once it is inside the body. It needs to be carried by two types of lipoproteins called low density lipoproteins(LDL) and high density lipoproteins(HDL). The more cholesterol we consume, the more LDL and HDL we produce. HDL is

The first biochemical phenotype resulting from inhibition of citrate lyase is the reduction of cholesterol in liver cells, resulting in increased amounts of LDL receptors on the cell surface. Increased number of LDL receptors increases the fractional catabolic rate of LDL particles circulating within the blood, thus reducing LDL-C levels. On another note, inhibiting citrate lyase leads to reduced levels of malonyl-CoA, leading to a switch from fatty acid synthesis to beta oxidation, limiting the synthesis of cholesteryl esters, triglycerides, and VLDL secretion. Reduced VLDL is likely to contribute to lower levels of

The lipoprotein gene mutation has a penetrance of greater than 90% (Henderson et al., 2016). Heterozygosity takes place when an individual has two dissimilar alleles of a gene. A single dominant gene can manifest itself in a heterozygous person particularly when there is high penetrance property. This is the reason why multiple generation can be affected by the FH disorder as seen in the proband and family members of the followed case discussion. Monogenic FH is largely attributed to mutations in the LDL-receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase, subtilisin/kexin-type 9 [PCSK9] genes (Brautbar et al.,

Heredity – Some people are born with a genetic pre-disposition to forming high cholesterol called familial hypercholesterolemia.

Atherosclerotic research has recently concentrated on inflammatory cytokines involved in vascular inflammation and how they stimulate the production of endothelial adhesion molecules, which could enter circulation in soluble form, and have the cytokines stimulate the production of messenger cytokine interleukin-6, which incites the liver production of acute-phase reactants such as C-reactive protein to increase. (Packard et al., 2007) In short, cytokines released into the bloodstream have a tendency to bring about an inflammatory response. Researchers have also found that that treatment with lipid-reducing agents is correlated with reduced morbidity and mortality from coronary heart disease and it seems to work near the atherosclerotic lesion, causing stabilization, slowed progression and, in some cases, regression of lesions. (Blankenhorn, 1989) In research it is well know that one human risk factor for atherosclerosis is hypercholesterolemia, which is when total cholesterol and low-density lipoprotein cholesterol are elevated. (Genis et al., 2000) There are more contributors and characteristics of hypercholesterolemia, which include inflammatory responses to oxidative stress,

Many forms of statins are present in the markets including atorvastatin (Lipitor), lovastatin (Mevacor, Altocor) and simvastatin (Zocor). Inhibition of 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG-CoA reductase), a key enzyme in the cholesterol biosynthetic pathway is the mode of action of most of the statins (2).

The LDL cholesterol inside of HDL and LDL particles is precisely the identical, it’s just that, for the maximum part, HDL is wearing it in one path and LDL is sporting it in the opposite route. The reason why LDL were dubbed horrific and HDL has been dubbed excellent is that numerous epidemiological studies most famously, the Framingham heart study told us that excessive LDL levels had been related to a better chance of heart assault, and that high HDL levels have been related to a lower risk of heart assault.

In vitro: In previous study, the authors proposed that LXRs could regulate the lipid metabolism via their interaction with specific oxysterols, such as 24(R)-hydroxycholesterol, 22(R)-hydroxycholesterol, 24(S)-hydroxycholesterol, and 24(S),25-epoxycholesterol. Results showed

Therefore, it needs to be transported through the blood stream by carriers, in this case, called lipoproteins. There are two main kind of lipoproteins, the low density lipoproteins (LDL) and the high density lipoproteins (HDL). The types of proteins are characterized as good or bad to the organisms. In this case the LDL is considered the bad cholesterol because it forms hard layers, that can obstruct the arteries and can make them less flexible to function properly. That is why HDL is considered to be beneficial one, since it as the scavenger that helps to remove the cholesterol from the arteries back to liver. Hence, the cells from those with FH show a deficiency in the number of functional LDL receptors, which at the same time cause the overproduction of cholesterol and a reduction in the ability to breakdown the protein in LDL (Rosenson et

While cholesterol is a commonly used word in healthcare, most people do not know what it means. Cholesterol is a “fat-soluble steroid alcohol that is produced in the liver from saturated fats and obtained from animal fats and oils in the diet” (Wells, 2012). Cholesterol is used to make certain hormones, like estrogen and testosterone, and aids in digesting fats. Cholesterol is a combination of a steroid ring structure and a hydroxyl group (Figure 1). It is important to note that there are two types of cholesterol: LDL, which is low-density lipoprotein and HDL which stand for high-density lipoprotein. LDL is considered the “bad cholesterol” because it contributes to fatty buildup in the arteries which can later lead to heart disease or a

Statins work by acting as a competitive inhibitor and competing for the binding pocket of the substrate HMG-CoA. This then causes a decrease in production of L-mevalonate, which then causes a decrease in the amount of cholesterol being produced. The decrease in cholesterol causes liver cells to signal for an up regulation of the low-density lipoprotein (LDL) receptors. This will then lead to an improved clearance of LDL-cholesterol from the

FH is a gloomy disorder with its genesis in early childhood resulting in damaging consequences in later life. Although the physical examination findings and lipid measurements are used to identify others who have inherited the disorder that are essential to reducing the risk of early cardiovascular disease, which is supportive to find out the common signs, such as xanthelasma, xanthoma, corneal arcus.

Then, there is a type of cholesterol that is referred to as “Bad Cholesterol” and may impact our health in a negative manner. The good type of cholesterol is called “HDL Cholesterol” and the bad type is referred to as “LDL Cholesterol”.

Lipocalins are a family of proteins which contribute various physiological role in small molecules. Lipocalins are found to take part in binding, storage or sequestration of many low molecular weight compounds which shows poor solubility and easy decomposition, thereby stabilizing them and playing an important role. In humans lipocalins are present as secretory proteins in blood, genital secretions and tears.