What Is Apoa-I Synthesis?

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

There are many risk factors which facilitate the development of atherosclerosis; abnormal level of blood lipids is just one of them. Blood lipids consisted of three components including cholesterol, triglycerides, and two major forms of lipoproteins: high density lipoproteins (HDLs) and Low density lipoproteins (LDLs). In addition, one of the critical components which determine the degree of blockage on the arterial walls is the quantity of

This gene instructs the body to make lecithin-cholesterol acyltransferase enzyme (LCAT enzyme) which has a function of removing cholesterol from body and tissues and carrying them to the liver by the help of lipoprotein molecules. The cholesterol molecules will then be redistributed to other body tissues or removed from body by the liver. The activity of LCAT enzymes which adds cholesterol molecules to high-density lipoprotein (HDL) is called Alpha-LCAT activity. When LCAT enzymes add cholesterol molecules to very low-density lipoprotein (VLDL) and low-density lipoprotein, the activity is called Beta-LCAT activity. The mutation in gene LCAT leads to the reducing of Alpha-LCAT activity in the LCAT enzyme. This results in body lacking cholesterol and cornea opacities cholesterol. There is so far no known reason why this mutation only causes cholesterol opacities in cornea (Fish-eye

Goldstein also studied that the level of LDL in the blood is inversely related to the LDLR activity. The LDL binds to the receptor via its principal surface protein called apolipoprotein B-100. The receptor, with it’s acquired LDL, then enters the call. This process is called Receptor-Mediated Endocytosis. When the number of functioning receptors is diminished because of a receptor mutation, LDL with its load of cholesterol

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

Fatty acids, monoglycerols, cholesterol, and apoprotein are packaged up to form cholymircons. Before the cholymicrons can move into the blood, they are transported through the lymphatics system. The cholymicrons are then transported through the blood which provide deliver lipids, and triglycerides to the tissues that need it for energy. The remaining cholymicrons will finish at the liver where they bind to LDL receptors which will allow for them to enter into the hepatic cells. In the liver, triglycerides can be formed and packaged into lipoproteins. Horowittz (2003) reported in the review article, that most fatty intra-abdominal adipose tissue contains the greatest lipolytic activity. Most of the fatty acids that are released from the intra-abdominal

There are three types of cholesterol: HDL (good cholesterol), LDL (bad cholesterol) and Triglycerides (contains natural fats and oils). HDL (high-density lipoprotein) cholesterol carries the cholesterol back to the liver to get broken down. LDL (low-density lipoprotein) cholesterol carries the cholesterol away from the liver into the bloodstream where it is likely to clog blood vessels. The buildup of the combination of Triglycerides with HDL or LDL in artery walls increases the risk for heart attack and stroke. Cholesterol level in the blood can be measured by fasting blood tests. Cholesterol level range is between 140 and 200 milligrams per deciliter. When cholesterol is too high the body would narrows, hardens, and blocks your arteries which increases the possibility of getting heart disease, heart attack or stroke, and plaque builds up in the arteries. When cholesterol is too low blood vessel will bursts and bleeds into the brain. It increases the risk of having anxiety, depression, preterm birth or premature birth. It will also damage or weaken the digestive system, brain, and liver. Cholesterol demonstrates homeostasis because it acts as a mechanism to maintain an internal steady state of cholesterol level within an organism by producing vitamin D, bile acids, and steroid hormones for the human

Early initiation of lipid-lowering therapy and lifestyle measures might modify the clinical outcome. These treatment initiatives have especially improved the prediction of HeFH. All of the medications used for heterozygous FH are also used to treat homozygous FH, such as bile acid absorbing resins, drugs “Shatins” are used. People with homozygous FH often undergo LDL apheresis, a process by which blood is removed through the patient’s vein and LDL is filtered out before the blood is passed back into a different vein, similar to dialysis. Some successful cases for homozygous FH patients undergo a liver transplant in order to normalize LDL levels, but homozygous FH is still harder to be treated. Therefore the nutrition therapy (lower cholesterol foods) is very important for the FH patients to focus on, which can manage the healthy lifestyle to avoid the bad cholesterol was

LDLR ko. mice. For therapeutic LDLR and VLDLR liver gene transfers, 50 LDLR knock-out (ko.) mice were fed a Western type (WT) high fat diet for two weeks for them to develop hyperlipidemic state, induce severe hypercholesterolemia, and initiate the progression of atherosclerosis. The study design had four parallel therapeutic gene transfer treatments versus controls. The SB elements were either co-administrated into mice livers in combination of SB100x and the T2/LSP-mLDLR or T2/LSP-mVLDLR transposon, or using the single ‘all-in-one’ plasmids. The T2/CAG-lacZ transposon vectors were used as gene transfer controls as the two promoters performed equally well in the in vitro testing when the respective T2/CAG-mLDLR and T2/LSP-mLDLR plasmid combinations were compared with each other and as the use of CAG promoter allowed performing a biodistribution study. Also, non-treated mice were included in the study. The mice were randomly divided into different treatment or control groups, and equal numbers of both sexes were selected for all groups. The littermates were divided into individual cages at the start of the high fat diet. To assess the normal blood lipid profiles the first blood samples were collected from randomly selected mice before they were put on a high fat diet. The second blood samples were collected two weeks later from all the mice to assess the ‘null blood samples on a WT diet’ before the gene transfers. The gene transfers were conducted using

Apo E2 allele act by delaying catabolism of lipoproteins that contain Apo E causing cholesterol of exogenous origin and periphery to enter the liver through Apo E mediated uptake then compensatory upregulation of LDL receptors occur resulting in enhanced uptake of LDL and additionally there is delay in the conversion of intermediate density lipids (IDL) to LDL all that causes decrease in level of total cholesterol and LDL level while Apo E4 show opposite so it associated with hypercholesterolemia (Anoop et al., 2010).

A mutation in the lipoprotein lipase gene causes this metabolic disorder and is inherited as a recessive trait. However, individuals who inherit a mutated gene and a normal gene (heterozygotes) are not at risk of the disorder. Interestingly, lipoprotein lipase deficiency is more prominent in Quebec, Canada, which is caused by a founder effect, where few individuals spawn a large population. In effect, lipoprotein deficiency causes improper fat digestion and accumulation of chylomicrons and triglycerides in the plasma, the fluid that suspends blood cells. When clogging occurs, the afflicted are at risk of atherosclerosis, as described in Figure 4. This clogging of the bloodstream can cause heart attack and stroke. It can also lead to acute pancreatitis, the inflammation of the pancreas and can extend to pancreatic insufficiency, the inability to digest food, as well as diabetes. Symptoms of lipoprotein lipase deficiency can be many; such conditions include abdominal pain, nausea, vomiting, loss of appetite, pale retinas and yellowing of eyes and skin (fatty deposits). In extremities, infants may fail to thrive with the disease. Lastly, treatment of lipoprotein lipase deficiency can be approached through low-fat diets, lipid powering drugs, and gene therapy. These treatments attempt to reduce pancreatitis attacks and cardiovascular diseases through nutrition-based therapy, allowing the body reduce its triglyceride concentrations. Further analysis of the structure and function of lipoprotein lipase will allow for improved treatments and

The fiber soluble has the ability to reduce the amount of bile reabsorbed in the intestines. The bile is excreted in the feces when fiber interferes with absorption of bile in the intestines,. To compensate with this loss of bile, the liver makes more bile salts. The body uses cholesterol to make bile salts. So in order to obtain the cholesterol necessary to make more bile salts, the liver increases its production of LDL receptors. These receptors are responsible for pulling cholesterol out of LDL molecules in the bloodstream. Therefore, the more bile salts are made from the liver, the more LDL cholesterol is pulled from the blood.

Lipitor a Statin drug, acts by inhibiting HMG-CoA reductase and are used as adjunct therapy to diet to reduce the risk of MI, stroke, revascularization procedures, angina , non-fatal MI, fatal and non-fatal stroke, hospitalization for CHF, reduce elevated total –C, apo B, and TG levels, increase HDL-C in adult patients with primary hyperlipidemia and mixed dyslipidemia, reduce total –C and LDL-C in patients with homozygous familial hypercholesterolemia and reduce elevated total –C and apo B levels in boys and postmenarchal girls 10-17 years of age with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. (Lipitor. 2012)

If our body produces more LDL than the requirement which is needed for the function of the cells, it builds up in our blood. This increase in LDL levels in the blood stream leads to process called atherosclerosis. Atherosclerosis is a condition in which the blood vessels are hardened.

Hypercholesterolemia induces the expression of several indicators of osteoblast differentiation and bone formation in the aorta, participating in VC. These characteristic molecules include the osteochondrogenic morphogens, BMP-2 and Wnt3a which are markedly up-regulated by HCD in aorta [13]. All these data support our findings that HCD intake for 12 wk significantly increased the genetic expression of BMP-2 and Wnt3a as well as calcium content in thoracic aorta, OCN level and ALP activity in serum of rabbits, suggesting VC. Our finding regarding BMP-2 was also confirmed by different previous studies which showed its expression in coronary artery endothelial cells in response to oxLDL-C [71], in human atherosclerotic lesions [72] and