Download (PDF, 786KB)

Lipoproteins core structure is made up of cholesterol esters and triglicerides, and the outer hydrophilic membrane of phospholipids, apoproteins, and free cholesterol; this allows the structure to move around the body and to be transported to cells that require them. LDL particles are thought to act as a major transporter of cholesterol, at least two-thirds of circulating cholesterol resides in LDL, to the peripheral tissues. Conversely, HDL molecules are thought to do the opposite, taking the excess cholesterol and return it into the liver for excretion.  Clinically, high LDL and low HDL increase the risk for CVDs such as atherosclerosis vascular diseases ^{[8], [9]}. GH treatment reduces plasma LDL cholesterol by inducing LDL clearance. In humans, LDLR expression is a prerequisite for this effect, whereas it is not related to stimulation of bile acid synthesis ^[10].

High density lipoprotein removes tissue cholesterol and helps its transport. Cholesterol ester present in HDL cholesterol is transferred and incorporated in to VLDL and LDL cholesterol. Hence high HDL-cholesterol level reflects protective action on the animals because of its scavenging action. According to the NHLBI, your risk for heart disease and other health problems, such as diabetes, increases if you have an HDL cholesterol level of 40 milligrams per deciliter (mg/dL) or less for men and 50 mg/dL or less for women. The institute recommends that total daily cholesterol intake be less than 200 mg/dL, and that LDL cholesterol be less than 100 mg/dL. The association of high cholesterol and triglicerides in blood increases the risk for CVD. Observational studies on population have demonstrated that high levels of LDL cholesterol and apolipoprotein B (apoB) 100, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE). Infiltration and the retention of apoB in the vascular wall initiates an inflammatory response and the promotion and development of atherosclerosis. An unresolved inflammation of the artery wall results of vulnerable ^{[11], [12]}.

An unresolved of the wall vessel inflammation results in necrotic cell death leading to an increased smooth muscle cell death, decreased extracellular matrix production, and collagen degradation by the protease of the macrophages. The rupture of the weak thinning fibrous cap will promote the formation of thrombus and eventually resulting in the clinical ischemic ASCVE ^[13]. Atherosclerotic plaque can break free from arterial walls or rupture and cause blood clots that can impede blood flow to the brain or heart. The result from this would be a stroke or heart attack. High fat content in diet increased blood cholesterol in rabbits. Along with high fat diet if some spices are also ingested, they are likely to influence blood cholesterol levels. This hike in blood cholesterol level is important in the development of atherosclerosis. Cholesterol is present not only in the free form in the blood but remarkable amount of cholesterol is transported as a component of different lipoproteins.

KEYWORDS:  Cardiovascular diseases, lipoprotein cholesterol, buckwheat, lipoprotein particles, Atherosclerotic plaque

Download (PDF, 714KB)