Fatty proteins that carry fat through the blood circulation to all vertebrates and even insects are compounds are soluble proteins (lipoproteins) and fat. In the liver is a fatty synthesis of proteins because of metabolic changes in the intestinal precursor. Cellular lipids and exogenous lipoproteins or lipoproteins are formed from lipoproteins or cell membranes. There is a complex cycle of proteins very fatty.

Are subject to the enzyme reactions to fatty acids, fat transfer operations assistance and spontaneous, and transfers of proteins intrinsic soluble, and changes to the composition of fatty proteins in response to changes synthetic. These proteins play a fatty function in the transfer of cholesterol and triglycerides, such as liver, muscle, and adipose tissue, are absorbed or absorbed from the place of origin to the place of use. Proteins Apo is the protein of fatty proteins part and helps in the transport and delivery process in three ways.

First, they have structural functions (for example, the protein protease B100 (Apo-B100) is the structural protein basic for VLDL and proteins fatty medium density (IDL) and LDL; Apo-A-I is the main structural protein for HDL). Second, these cells operate in the form of links to the receptor (for example, targets Apo-B LDL for the future of LDL on the liver and peripheral tissues; Apo-E is also linked to the future of LDL which is important to identify the remains of the liver). Third, the fatty protein cofactors (Apo-C-II is a working assistant agent for fatty protein lipase, for example, and Apo-A-I is an assistant factor that is a lecithin cholesterol acyltransferase (LCAT).

Structure and Classification of Lipoproteins

A lipoprotein particle is a mature ball consists of a surface layer phospholipid, and cholesterol is unstable and is surrounded by fatty proteins central nuclei (triple fat and cholesterol esters) (apoproteins) (Figure 1). In practical terms, you can identify fatty proteins based on the size and characteristics of buoyancy.

Structure and Classification of Lipoproteins

1. Chylomicrons (CM)
The majority of the lipoprotein particles are CMs. The main structural protein is Apo-B-48. Triglycerides are the bulk (80%) of core lipids. These molecules are manufactured and secreted from the intestine and maintain external cholesterol, fatty acids, vitamins, and fat-soluble from digested foods.

Is synthesized and secreted by the liver, and this particle-rich triple-fat (80% of central fat is triglycerides) is the introduction of fatty proteins medium density (IDL) and LDL. The main structural protein is Apo-B-100.

The residue (VLDL) is formed from the lipoprotein lipase after the degradation of triglycerides in VLDL. Essential fats are made up of about 50 percent triglycerides and 50 percent of cholesterol ester. In clinical practice, the measurement of LDL and includes cholesterol fractions IDL and LDL.

The main structural protein is central Apo-A-I and lipids are also mainly cholesteryl ester. One of the functions in the transport of fatty proteins E and C-II between chylomicrons VLDL and HDLIt also play an opposite role to atherosclerosis LDL by helping to remove cholesterol in the tissue transfer method of reverse cholesterol. (not included in Figure2) The size of fatty proteins and characteristics of the floats


This lipoprotein is the result of treating hepatic VLDL residues. Central fats, which represent a lot of cholesterol, circulate in the blood that is rich in cholesterol esters. It plays a major part in atherosclerosis promoting.

Lipoproteins Physiology:

Apo-B-100 is synthesized in the liver, in the endoplasmic reticulum. Most of this is locally degraded Apo-B. Apo-B is transported to the Golgi, where core lipids are inserted, destined to be secreted as VLDL. VLDL particle appearance (early) in plasma (Figure 3). Where they are getting fatty proteins from high-density lipoproteins, such as Apo-C-II and Apo-E.

VLDL particle appearance early in plasma

Lipoproteins Pathophysiology

Two genetic variants of hyperlipidemia can cause defects in VLDL secretion: familial hypertriglyceridemia and familial combined hyperlipidemia. The overproduction of triglycerides is characterized by individuals with familial hypertriglyceridemia, The effect is a typical number of VLDL particles per particle with an excessive amount of triglycerides. On the other hand, people who suffer from excessive blood mixed hyperlipidemia family primarily excessive Apo-B100 in the VLDL and/or particles that LDL containing normal amounts of fat and cholesterol triple (Figure 1.8.). The molecular basis of fat triple and excessive production of Apo-B in these circumstances is unclear.

Lipoprotein (a):

Plasma lipoprotein human Lp (a) is a macromolecular complex first identified by the Norwegian physician Kåre Berg in 1963. Lipoprotein(a), a liver-synthesized particle consisting of a covalently bound apolipoprotein B100 (Apo B100) molecule to a very large glycoprotein known as apolipoprotein, is now considered to represent a distinct genetic form of low-density lipoprotein (LDL), Apo A is Lp (a) is connected by a second private links disulfide A poB100B100.

Believes that Apo A reaction residues cysteine is identified at the end of carboxyl’s happening in apoB100 K4366 through the remains of cystine is not associated. This explains why the correlation ApoB4a, a type of intestinal Apo B, which lacks the carboxyl end for ApoB100, Lp (a). It was found Lp (a) also in terms of size and density to be heterogeneous. Protein differences may be responsible for this variation: fat, ApoB100: stoichiometric for Apo A, and scale Apo (a ratio) multi-forms, which ranges from 300 to 800 kDa.

Although very small differences between individuals, the multiplicity of forms of scale Apo (a) may be one of the factors behind a wide range of differences between individuals in the plasma levels of Lp (a) that up to 1000 times. Despite all these protein-level dilemmas and mysteries about the mechanisms of the adverse effects of Lp(a) on cardiovascular outcomes, good human genetic and epidemiological evidence supports the causal function of Lp(a) in cardiovascular arteriosclerotic disease and provide one of the best-supported genetic ties to aortic stenosis that have arisen from genome-wide association.