Blood lipid include cholesterol and triglycerides. Causing serious harm is mainly cholesterol abnormalities, in particular, LDL-C (low-density lipoprotein) are excessive. Studies have shown that failure to show an increase in triglyceride and coronary heart disease, ischemic cardiovascular disease associated with an increased relative risk.
And if there is too much blood low-density lipoprotein deposition in the arterial wall, it will form a plaque. There plaque rupture of blood vessels narrow or directly lead to acute myocardial infarction, stroke and even sudden death. Therefore, low-density lipoprotein cholesterol is the most important indicators of blood lipid testing, not triglycerides.
Triglycerides as the international community did not refer to hyperlipidemia disorder, more recent emphasis on triglycerides, if the triglyceride numbers used to calculate mg, 150 mg is equivalent to 1.7mmol / L, this figure is below normal range, if it exceeds more than this figure is not very good, and now more than clinical triglycerides did not say how much in need of treatment, but now there is an observation, when the triglyceride is equivalent to 200 mg of 2.1mmol / L or so, even if the normal low-density lipoprotein, high-density lipoprotein is normal, the risk of heart disease has increased from one to two times. If the triglyceride to 2.1mmol / L (200 mg) or more, low-density lipoprotein or high-density lipoprotein high-low, then the incidence of heart disease can increase three to four times. This is a well-known recent research findings, this result reminds us that attention should be paid triglycerides, triglyceride standard difficult to determine how much it must be treated, but if high triglyceride must be focus, more mainly depends on low-density lipoprotein is high and your HDL is low.
Blood lipids include cholesterol (or total cholesterol TC) and triglycerides in the blood circulation in the presence of non-free state, and the protein binding of macromolecules such as lipoprotein transport. The major lipoprotein categories — chylomicrons, very low density (pre-?) lipoprotein (VLDL), low density (?-) lipoprotein (LDL), and high-density (a-) lipoprotein (HDL) — these proteins are closely related, while the classification often on the physical and chemical properties (for example, electrophoretic mobility rate and the density ultracentrifugation after the separation). blood lipoprotein transport of the major triglycerides, lipoprotein chylomicrons is the largest carriers of exogenous sweet 3 ester oil through the thoracic duct into the venous system, the capillaries in the fat and muscle tissue, 90% of chyle triglycerides through a specific set of esterase were diverted, chylomicrons are hydrolyzed into fatty acids and glycerol into the fatty cells and muscle cells have been used or stored, this lipase quickly so that the endogenous VLDL triglyceride degradation, caused by medium-density lipoprotein (IDL) loss of triglyceride and apo-protein, 2 ~ 6 hours more of IDL through separation and further degradation of triglycerides into LDL, LDL in the plasma half-life of 2 ~ 3 days, VLDL is the main source of plasma LDL.
The excretion of LDL is not very clear, the liver removed about 70%, there are active receptor site to remove circulating in the majority of LDL, these loci in the liver cells and specific and apolipoprotein B (apoB) with the cell surface, and the LDL associated ligand, LDL, and LDL receptor-binding capacity is very small but important part of the LDL has been circulating in the bypass of the non-LDL receptor, clearance, including the macrophage receptors on the intake, remove macrophage to move to the arterial walls become foam cells in atherosclerosis plaque.
Hyperlipidemia VLDL produced by too much or to remove barriers, as well as the oversupply of VLDL into LDL. Obesity, diabetes, alcohol excess, nephrotic syndrome, or genetic defects can cause the liver VLDL to produce too much, LDL and TC are usually of higher associated with high triglycerides and blood. LDL removal of obstacles and the structure of apoB defects. In addition, remove obstacles may also be due to reduce the number of LDL receptors or functional abnormalities (lower energy), which may be genetic or dietary factors. LDL receptor protein molecular defect structure of LDL receptor dysfunction is a common genetic cause — a common mechanism of genetic defects will be described below.
When the dietary cholesterol (chylomicrons remnants part) to reach the liver, the rise of intracellular cholesterol (or cholesterol metabolism of liver cells) increased inhibition of the LDL-receptor synthesis, also inhibited the LDL gene transcription, receptor caused a decline in the number of plasma LDL and TC levels increased. Unsaturated fatty acids will also enable increased levels of plasma LDL and TC, mechanism for it to decline in LDL receptor function. In the United States, the Food and cholesterol and a high intake of saturated fatty acids, LDL plasma levels of up to 25 ~ 40mg/dl (0.65 ~ 1.03mmol / L) — which makes the incidence of coronary heart disease significantly increased.