20. 載脂蛋白 A
載脂蛋白 A-I
載脂蛋白 A-II
載脂蛋白 A-IV
載脂蛋白 A-V
載脂蛋白 B
載脂蛋白 B 48
載脂蛋白 B100
載脂蛋白 C
載脂蛋白 C-I
載脂蛋白 C-II
載脂蛋白 C-III
載脂蛋白 C-IV
載脂蛋白 D
載脂蛋白的分類
載脂蛋白有六個主要的分類以及若干子分類：
21. 常見的載脂蛋白
種類 附著的脂蛋白 功能
Apo A-I HDL 、 chylomicron
s
1. 回收膽固醇運送回肝臟
2. 活化 LCAT(lecithin cholesterol
acyltransferase)
3. 作為 HDL 的受體配基 (ligand)
Apo B-100 LDL 、 VLDL 、 IDL
( 僅出現在三個 )
1. 從肝臟中釋放 VLDL
2. 作為 LDL 的受體配基
Apo B-48 Chylomicrons 、 Ch
ylomicron 剩餘物
從小腸中釋放乳糜微粒
Apo C-I VLDL 、 HDL 、 chy
lomicrons
活化 LCAT
Apo C-II 活化血管上的 lipoprotein lipase
Apo C-III 抑制 Apo C-II
Apo E 存在所有的脂蛋白中 1. 作為乳糜微粒代謝後剩餘物受體的
配基
2. 作為 LDL 受體的配基
22. 載脂蛋白的功能
功能 例子
為脂蛋白結構的一部分 Apo B
作為酵素的輔因子
(cofactors)
Apo C-II 脂蛋白脂解脢 (lipoprotein lipase)
Apo A-I 卵磷脂膽固醇醯基轉移酶
(lecithin ： cholesterol
acyltransferase ， LCAT)
為酵素的抑制劑
(inhibitors)
Apo A-II Apo
C-III
脂蛋白脂解脢 (lipoprotein lipase)
Apo C-I 膽固醇酯轉移蛋白 (cholesteryl
esters transferase)
作為組織間脂蛋白上受體
(receptor) 的配基 (ligand)
Apo B-100
Apo E
LDL receptor
Apo A-I HDL receptor
作為脂質轉移蛋白
(Lipid transfer proteins)
Apo D HDL
Many enzymes,transporters, structural proteins, antigens, adhesins, and toxins are lipoproteins.
Examples include the plasma lipoprotein particles classified under high-density (HDL) and low-density (LDL) lipoproteins, which enable fats to be carried in the blood stream, the transmembrane proteins of the mitochondrion and the chloroplast, and bacterial lipoproteins.
A core of fats (triglycerides), cholesterol esters (cholesterol linked to fatty acids), and fat-soluble vitamins.
A monolayer membrane of phospholipids and small amounts of free cholesterol.
Proteins called “apoprotein” which may be “integral” apoproteins (apoA or apoB) penetrating as a transmembrane protein through the monolayer membrane, compared to the “peripheral” apoproteins (apoC or apoE) that are on the outer surface of the phospholipid membrane.
A core of fats (triglycerides), cholesterol esters (cholesterol linked to fatty acids), and fat-soluble vitamins.
A monolayer membrane of phospholipids and small amounts of free cholesterol.
Proteins called “apoprotein” which may be “integral” apoproteins (apoA or apoB) penetrating as a transmembrane protein through the monolayer membrane, compared to the “peripheral” apoproteins (apoC or apoE) that are on the outer surface of the phospholipid membrane.
A core of fats (triglycerides), cholesterol esters (cholesterol linked to fatty acids), and fat-soluble vitamins.
A monolayer membrane of phospholipids and small amounts of free cholesterol.
Proteins called “apoprotein” which may be “integral” apoproteins (apoA or apoB) penetrating as a transmembrane protein through the monolayer membrane, compared to the “peripheral” apoproteins (apoC or apoE) that are on the outer surface of the phospholipid membrane.
A core of fats (triglycerides), cholesterol esters (cholesterol linked to fatty acids), and fat-soluble vitamins.
A monolayer membrane of phospholipids and small amounts of free cholesterol.
Proteins called “apoprotein” which may be “integral” apoproteins (apoA or apoB) penetrating as a transmembrane protein through the monolayer membrane, compared to the “peripheral” apoproteins (apoC or apoE) that are on the outer surface of the phospholipid membrane.
A core of fats (triglycerides), cholesterol esters (cholesterol linked to fatty acids), and fat-soluble vitamins.
A monolayer membrane of phospholipids and small amounts of free cholesterol.
Proteins called “apoprotein” which may be “integral” apoproteins (apoA or apoB) penetrating as a transmembrane protein through the monolayer membrane, compared to the “peripheral” apoproteins (apoC or apoE) that are on the outer surface of the phospholipid membrane.
The lipid components of lipoproteins are insoluble in water. However, because of their detergent-like (amphipathic) properties, apolipoproteins and other amphipathic molecules (such as phospholipids) can surround the lipids, creating the lipoprotein particle that is itself water-soluble, and can thus be carried through water-based circulation (i.e., blood,lymph).
脂蛋白中的脂質是不溶於水。然而，由於它們的洗滌劑般（兩親性）的特性，載脂蛋白和其它兩親分子（例如磷脂）可以包裹著脂質，製造出本身是水溶性的脂蛋白顆粒，因此可以在水中（即血液，淋巴液）進行循環。
Chylomicrons are the lipoprotein packages transporting fat from our diet to adipose tissue in our body and the liver.
乳糜微粒是一種脂蛋白我們的身體和肝臟中運輸從我們的飲食中獲取的脂肪到脂肪組織。
Chylomicrons are the lipoprotein packages transporting fat from our diet to adipose tissue in our body and the liver.
乳糜微粒是一種脂蛋白我們的身體和肝臟中運輸從我們的飲食中獲取的脂肪到脂肪組織。
Our intestines package cholesterol, fats, and fat-soluble nutrients and vitamins into chylomicrons in the enterocyte cell lining the small intestine.
我們的小腸組裝膽固醇、脂肪、脂溶性營養物質和維生素在小腸細胞形成乳糜微粒。
The apoprotein that these lipoproteins get is apoB-48.
這些脂蛋白得到的載脂蛋白是Apo B-48。
Chylomicrons are the lipoprotein packages transporting fat from our diet to adipose tissue in our body and the liver.
乳糜微粒是一種脂蛋白我們的身體和肝臟中運輸從我們的飲食中獲取的脂肪到脂肪組織。
Our intestines package cholesterol, fats, and fat-soluble nutrients and vitamins into chylomicrons in the enterocyte cell lining the small intestine.
我們的小腸組裝膽固醇、脂肪、脂溶性營養物質和維生素在小腸細胞形成乳糜微粒。
The apoprotein that these lipoproteins get is apoB-48.
這些脂蛋白得到的載脂蛋白是Apo B-48。
Chylomicrons enter the lymphatic circulation and make their way via the thoracic lymph duct to the circulation where the duct empties into the subclavian vein in the neck.
乳糜微粒進入淋巴循環，並經由胸淋巴導管到循環使他們的方式，其中導管匯入在頸部鎖骨下靜脈。
The chylomicrons travel either to the liver or adipose tissue.
乳糜微粒被運送到肝或脂肪組織。
In the blood stream the chylomicrons acquire two new apoproteins, both peripheral apoproteins; apoC and apoE.
在血液中乳糜微粒獲得兩個新的載脂蛋白，無論是外圍的蛋白質;載脂蛋白E和載脂蛋白E。
The chylomicron will also bind preferentially to adipocytes via the apoC lipoprotein to lipoprotein lipase (LPL) an enzyme on the surface of the adipocyte.
乳糜微粒通過載脂蛋白C與脂肪細胞的表面上的脂蛋白脂酶(lipoprotein lipase, LPL)與脂肪細胞相結合。
The LPL cleaves the triglycerides in the chylomicron and the glycerol and free fatty acids enter the adipocyte thus depleting the chylomicron of triglyceride content and filling the fat cell with fatty acids.
LPL會將乳糜微粒中的甘油三酸酯切割成為甘油和游離脂肪酸並進入脂肪細胞，從而消耗乳糜微粒中甘油三酯的含量和填充脂肪酸到脂肪細胞。
When triglyceride is reduced to ~ 20% in the chylomicron the apoC dissociates from the chylomicron and this reduced triglyceride lipoprotein with only apoB48 and apoE is now called a “chylomicron remnant”.
當乳糜微粒中的甘油三酯降低到〜20％時，載脂蛋白C從乳糜微粒解離，此時的糜微粒解僅存有載脂蛋白B 48和載脂蛋白E並被稱為“乳糜微粒殘餘” (chylomicron remnant)。
The chylomicron remnant is cleared from the circulation by the liver cell (hepatocytes) via the chylomicron remnant receptor on the hepatocytes, binding to the apoE on the remnant particle. The liver then makes use of the remaining triglyceride.
乳糜微粒殘餘通過ApoE與肝細胞的乳糜微粒殘餘受體(chylomicron remnant receptor)結合，進入循環中進行清除。肝臟然後利用剩餘的甘油三酯。
The chylomicrons travel either to the liver or adipose tissue.
乳糜微粒被運送到肝或脂肪組織。
極低密度脂蛋白（VLDL）將（新合成的）甘油三酯從肝臟帶往脂肪組織。
The chylomicrons travel either to the liver or adipose tissue.
乳糜微粒被運送到肝或脂肪組織。
The chylomicrons travel either to the liver or adipose tissue.
乳糜微粒被運送到肝或脂肪組織。
The chylomicrons travel either to the liver or adipose tissue.
乳糜微粒被運送到肝或脂肪組織。
VLDL carries mainly triglyceride and cholesterol ester (see table above) and the each VLDL containing one apoB100 integral apoprotein in the monolayer membrane.
Nascent 發生中的,開始存在的,初期的
脂蛋白脂肪酶（lipoprteinlipase，LPL）是脂肪細胞、心肌細胞、骨骼肌細胞、乳腺細胞以及巨噬細胞等實質細胞合成和分泌的一種糖蛋白。
Again identical to chylomicrons the VLDL binds the adipocyte via the apoC to LPL on the adipocyte with the enzyme cleaving the triglyceride to glycerol and fatty acids to be used by the adipocyte.
再次相同乳糜微粒的VLDL結合經由載脂蛋白C到LPL上與酶裂解甘油三酯為甘油和由脂肪細胞中使用的脂肪酸的脂肪細胞的脂肪細胞。
Once in circulation, VLDL will come in contact with lipoprotein lipase (LPL) in the capillary beds in the body (adipose, cardiac, and skeletal muscle).
LPL will remove triglycerides from VLDL for storage or energy production.
VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides via cholesterylester transfer protein(CETP).
VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides via cholesterylester transfer protein(CETP).
VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides via cholesterylester transfer protein(CETP).
As the triglyceride in the VLDL drops to 50% the VLDL dissociates from the LPL and returns to the liver binding to the LDL-receptor (LDL-R) via the apoE on the VLDL.
當VLDL中的甘油三酯下降到50％時，VLDL會與LPL解離，並經由Apo E與低密度脂蛋白受體（LDL-receptor, LDL-R）結合而返回到肝臟。
If the VLDL attached to the adipocyte stays attached longer or attaches to another adipocyte and depletes the triglyceride to 30% the lipoprotein becomes an IDL molecule which is triglyceride depleted and thus has more percent cholesterol ester.
如果連接到脂肪細胞的VLDL附著時間較長或附著到另一個脂肪細胞而造成三酸甘油酯耗用至30％，此時的脂蛋白變成一個IDL分子，其中的甘油三酯耗盡因此具有更多的膽固醇酯。
As more and more triglycerides are removed from the VLDL because of the action of LPL and CETP enzymes, the composition of the molecule changes, and it becomes intermediate-density lipoprotein (IDL).
VLDL is a large, triglyceride-rich lipoprotein secreted by the liver that transports triglyceride to adipose tissue and muscle. VLDL是由輸送甘油三酯脂肪組織和肌肉肝臟分泌的一種大的，富含甘油三酯的脂蛋白。
The triglycerides in VLDL are removed in capillaries by the enzyme lipoprotein lipase, and the VLDL returns to the circulation as a smaller particle with a new name, intermediate-density lipoprotein (IDL). 在VLDL甘油三酯的毛細血管由酶脂蛋白脂肪酶被除去，VLDL返回到循環作為一個更小的顆粒用一個新名稱，中密度脂蛋白（IDL）。
If the VLDL attached to the adipocyte stays attached longer or attaches to another adipocyte and depletes the triglyceride to 30% the lipoprotein becomes an IDL molecule which is triglyceride depleted and thus has more percent cholesterol ester.
如果連接到脂肪細胞的VLDL附著時間較長或附著到另一個脂肪細胞而造成三酸甘油酯耗用至30％，此時的脂蛋白變成一個IDL分子，其中的甘油三酯耗盡因此具有更多的膽固醇酯。
極低密度脂蛋白（VLDL）將（新合成的）甘油三酯從肝臟帶往脂肪組織。
Intermediate-density lipoproteins (IDLs) belong to the lipoprotein particle family and are formed from the degradation of very low-density lipoproteins.
中密度脂蛋白（Intermediate-density lipoprotein, LDL）為五種主要的脂蛋白中的其中一種，是從極低密度脂蛋白的降解而形成。
IDL是VLDL分解成LDL的過程中，分解速度緩慢下來時才會產生的中間產物。它的性質介於VLDL與LDL之間，具有將脂質（主要是膽固醇和中性脂肪）運送到末梢組織的作用。
Intermediate-density lipoproteins (IDLs) belong to the lipoprotein particle family and are formed from the degradation of very low-density lipoproteins.
中密度脂蛋白（Intermediate-density lipoprotein, LDL）為五種主要的脂蛋白中的其中一種，是從極低密度脂蛋白的降解而形成。
IDL是VLDL分解成LDL的過程中，分解速度緩慢下來時才會產生的中間產物。它的性質介於VLDL與LDL之間，具有將脂質（主要是膽固醇和中性脂肪）運送到末梢組織的作用。
Intermediate-density lipoproteins (IDLs) belong to the lipoprotein particle family and are formed from the degradation of very low-density lipoproteins.
中密度脂蛋白（Intermediate-density lipoprotein, LDL）為五種主要的脂蛋白中的其中一種，是從極低密度脂蛋白的降解而形成。
IDL是VLDL分解成LDL的過程中，分解速度緩慢下來時才會產生的中間產物。它的性質介於VLDL與LDL之間，具有將脂質（主要是膽固醇和中性脂肪）運送到末梢組織的作用。
Their size is, in general, 25 to 35 nm in diameter, and they contain primarily a range of triacylglycerols and cholesterol esters.
它們的尺寸是，在一般情況下，25至35納米的直徑，並且它們主要包含一個範圍甘油三酯和膽固醇酯組成。
中間密度脂蛋白（IDL）的密度和大小介於極低密度脂蛋白與低密度脂蛋白之間。在血液中常檢測不到他們的存在。
The IDL particles have lost most of their triglyceride, but they retain cholesteryl esters. IDL的顆粒已經失去了大部分的甘油三酯，但他們保留膽固醇酯。
Some of the IDL particles are rapidly taken up by the liver; others remain in circulation, where they undergo further triglyceride hydrolysis and are converted to LDL. 一些在IDL顆粒被迅速被肝臟;更為仍在流通，這裡它們經受進一步的甘油三酯水解，並轉化成LDL。
They are cleared from the plasma into the liver by receptor-mediated endocytosis, or further degraded to form LDL particles.
IDL從血漿中清除通過受體介導的內吞作用(receptor-mediated endocytosis)進入肝臟，或進一步降解以形成LDL(約有50%)。
IDL在血漿中的濃度很低，約有50%的IDL將進一步代謝成LDL。
The IDL particles have lost most of their triglyceride, but they retain cholesteryl esters. IDL的顆粒已經失去了大部分的甘油三酯，但他們保留膽固醇酯。
Some of the IDL particles are rapidly taken up by the liver; others remain in circulation, where they undergo further triglyceride hydrolysis and are converted to LDL. 一些在IDL顆粒被迅速被肝臟;更為仍在流通，這裡它們經受進一步的甘油三酯水解，並轉化成LDL。
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Fifty percent of IDLs are recognized by receptors in the liver cells because of the apolipoprotein B-100 (apoB-100) and apoE they contain and are endocytosed.
The IDL is taken up by the liver by the LDL-R via apoE.
一些進入循環，這裡它們經受進一步的甘油三酯水解(triglyceride hydrolysis)，並轉化成LDL。
The other 50% of IDL lose apoE; when their cholesterol content becomes greater than the content of triglyceride, they become LDL, with apoB-100 as the primary apolipoprotein.
IDL can also rebind to adipocytes to deplete itself more of its triglyceride to ~ 10% where the IDL loses the apoE and apoC peripheral apoproteins and becomes a cholesterol ester rich LDL molecule with only one apoB100 apoprotein per LDL molecule.
The LDL is taken into a cell via the LDL receptor via endocytosis, where the contents are either stored, used for cell membrane structure, or converted into other products such as steroid hormones or bile acids.
極低密度脂蛋白（VLDL）將（新合成的）甘油三酯從肝臟帶往脂肪組織。
So LDL looks similar to VLDL with a single apoB100 apoprotein but unlike the VLDL that is triglyceride rich the LDL is cholesterol ester rich and is the MAIN carrier lipoprotein to transport cholesterol via its ester to the liver and other cells throughout the body.
所以LDL類似於VLDL，但LDL只有一個Apo B100載脂蛋白，而且不像是富含甘油三酯的VLDL，LDL是富含膽固醇酯，是運輸膽固醇到肝臟和其他身體的細胞的主要載脂蛋白。
Importantly the LDL molecule does not have apoE or apoC and is therefore not cleared from the blood by the liver as the LDL-R has high affinity for the apoE.
重要的是低密度脂蛋白分子不具有載脂蛋白E或載脂蛋白C，因此不從血液由肝臟作為LDL-R的清除具有用於載脂蛋白E高的親和力。
The apoB100 in LDL has a much lower affinity for the LDL-R on the hepatocytes and as a result the ½ life of LDL in the blood is much longer than all the other lipoproteins like VLDL; IDL both of which have apoE to bind the LDL-R on the liver cell.
LDL中Apo B100對於在肝細胞表面的LDL-R具有較低的親和力，結果是1/2的LDL在血液中的壽命比其他所有脂蛋白如VLDL和LDL長得多;這兩者都具有Apo E能與肝細胞的LDL-R相結合。
Importantly the LDL molecule does not have apoE or apoC and is therefore not cleared from the blood by the liver as the LDL-R has high affinity for the apoE.
重要的是低密度脂蛋白分子不具有載脂蛋白E或載脂蛋白C，因此不從血液由肝臟作為LDL-R的清除具有用於載脂蛋白E高的親和力。
The apoB100 in LDL has a much lower affinity for the LDL-R on the hepatocytes and as a result the ½ life of LDL in the blood is much longer than all the other lipoproteins like VLDL; IDL both of which have apoE to bind the LDL-R on the liver cell.
LDL中Apo B100對於在肝細胞表面的LDL-R具有較低的親和力，結果是1/2的LDL在血液中的壽命比其他所有脂蛋白如VLDL和LDL長得多;這兩者都具有Apo E能與肝細胞的LDL-R相結合。
The consequence of the long ½ life of LDL in the plasma is the LDL is susceptible to oxidative modification of the phospholipid monolayer containing polyunsaturated fatty acids.
血漿中LDL的長半生命的後果是低密度脂蛋白易受含多不飽和脂肪酸的磷脂單層的氧化修飾。
This is where the MISNOMER arises with LDL labelled as the “BAD” cholesterol.
LDL is just the main carrier of cholesterol required by all cells in the body.
It is NOT the cholesterol that is atherogenic (causing atherosclerosis), it is the damaged oxidized LDL lipoprotein that is taken up by macrophages in the sub endothelial space of the arterial lining.
這就是將LDL標記為“壞”膽固醇用詞不當的產生。
LDL只是體內所有細胞所需的膽固醇的主要載體。
這並不是說膽固醇是致動脈粥樣硬化（引起動脈粥樣硬化），而是受損氧化的LDL脂蛋白在動脈內層的子內皮空間中被由巨噬細胞所吞噬。
The problem is that LDL is our carrier of cholesterol and so high LDL particularly when oxidized is directly associated with high risk for vascular disease.
問題在於LDL是膽固醇的載體和當氧LDL的數量特別高時直接與血管疾病的高風險有關。
LDL (the main cholesterol rich) lipoprotein and if it spends too long in the circulation by poor hepatic uptake tends to oxidize. The polyunsaturated fatty acids (PUFA) in its membrane get damaged by free radicals, and then they proceed to damage the protein in the surface, and finally the fatty acids in the core.
LDL（主要富含膽固醇）的脂蛋白，如果因為肝臟的攝取不良而導致花費太長在體內循環則容易氧化。自由基會對LDL膜上的多元不飽和脂肪酸（PUFA）進行損壞，然後繼續損害表面上的蛋白質，最後是在核心中的脂肪酸。
LDL (the main cholesterol rich) lipoprotein and if it spends too long in the circulation by poor hepatic uptake tends to oxidize. The polyunsaturated fatty acids (PUFA) in its membrane get damaged by free radicals, and then they proceed to damage the protein in the surface, and finally the fatty acids in the core.
LDL（主要富含膽固醇）的脂蛋白，如果因為肝臟的攝取不良而導致花費太長在體內循環則容易氧化。自由基會對LDL膜上的多元不飽和脂肪酸（PUFA）進行損壞，然後繼續損害表面上的蛋白質，最後是在核心中的脂肪酸。
Once LDL oxidizes, it can invade the arterial wall in areas that experience disturbed blood flow (turbulence), like the points where arteries curve or branch. These areas are permeable to large molecules. Oxidized LDL attracts immunocompetent white blood cells (to repair the artery) and initiate an inflammatory cascade that produces the unstable arterial plaque. This is the basis of the “oxidized LDL theory of atherosclerosis”.
一旦LDL氧化，它可以侵入到遇到干擾的血流量（動盪）區域的動脈壁，例如動脈曲線或分支的地方。這些區域是可以被大分子所滲透。氧化LDL吸引免疫白血細胞（以修復動脈）並啟動炎症連鎖反應產生不穩定動脈斑塊。這是“動脈粥樣硬化的氧化LDL理論”的基礎。
Once LDL oxidizes, it can invade the arterial wall in areas that experience disturbed blood flow (turbulence), like the points where arteries curve or branch. These areas are permeable to large molecules. Oxidized LDL attracts immunocompetent white blood cells (to repair the artery) and initiate an inflammatory cascade that produces the unstable arterial plaque. This is the basis of the “oxidized LDL theory of atherosclerosis”.
一旦LDL氧化，它可以侵入到遇到干擾的血流量（動盪）區域的動脈壁，例如動脈曲線或分支的地方。這些區域是可以被大分子所滲透。氧化LDL吸引免疫白血細胞（以修復動脈）並啟動炎症連鎖反應產生不穩定動脈斑塊。這是“動脈粥樣硬化的氧化LDL理論”的基礎。
Large LDL particles measure around 27 nm in diameter, while small LDL particles measure around 24 nm.
smaller LDL particles having greater triglyceride content and less cholesterol.
小而密的LDL顆粒含有較多的甘油三酯含量和較少的膽固醇含量。
smaller LDL particles having greater triglyceride content and less cholesterol.
小而密的LDL顆粒含有較多的甘油三酯含量和較少的膽固醇含量。
smaller LDL particles having greater triglyceride content and less cholesterol.
小而密的LDL顆粒含有較多的甘油三酯含量和較少的膽固醇含量。
--Are not cleared from the bloodstream as rapidly as the more normal large LDL particles, since the LDL receptor recognizes them less effectively.
--Are不能從血液中盡可能快的比較正常的大LDL顆粒被清除，因為LDL受體較少有效地識別它們。
Small LDL of pattern B therefore hang around much longer, providing more opportunity to cause atherosclerotic plaque.
因此，模式B的小LDL流連更長的時間，提供更多的機會，引起動脈粥樣硬化斑塊。
--Are more adherent to the artery wall, making them more likely to trigger plaque formation.
--Are更多粘附到動脈壁，使他們更可能觸發斑塊的形成。
--Are more potent triggers of inflammatory responses of the sort that make atherosclerotic plaque grow.
--Are的，使粥樣硬化斑塊成長的那種炎症反應更有力的觸發器。
--Are more prone to oxidation, making them more powerful triggers of inflammation.
--Are更容易氧化，使得它們更強大的炎症的觸發器。
--Are more prone to glycation, or the glucose-triggered modification of the apoprotein B that makes it much more likely to contribute to atherosclerotic plaque.
--Are更容易發生糖化，或因葡萄糖觸發修改載脂蛋白B的，使得它更可能有助於動脈粥樣硬化斑塊。
醣化（glycation）是在不受酶的控制下，蛋白質或脂質分子上附加糖類分子（如果糖或葡萄糖）的過程。
A special blood test called polyacrylamide gradient gel electrophoresis can measure particle size and determine whether a person has blood cholesterol LDL pattern A or LDL pattern B.
一個特殊的驗血叫聚丙烯酰胺梯度凝膠電泳可以測量顆粒的大小，並確定一個人血液中的膽固醇是LDL模式A或LDL模式B。
Individuals with pattern B are also more likely to develop high blood triglyceride levels after a fatty meal (postprandial hyperlipidemia).
具有模式B的個體在吃完一頓富含脂肪的餐後容易發生高血甘油三酯水平(餐後高脂血症)。
Pattern B is associated with accelerated atherosclerosis and a 3 to 5- fold increase in heart attack risk. 模式B的個體與加速動脈粥樣硬化有關聯，並在心臟病發作的風險增長3到5倍。
Pattern B is believed to be the most important cause of atherosclerosis in people with normal or near normal total and LDL cholesterol levels.
在有著正常或接近正常的總膽固醇和LDL膽固醇水平的人群中，模式B被認為是導致動脈粥樣硬化最重要的原因。
Some scientists believe that the smaller LDL particles are more dangerous than the larger ones because they can more easily squeeze through the tiny gaps between the cells in the endothelium to reach inside the artery walls.
一些科學家認為，較小的LDL顆粒比較大的更加危險，因為他們可以通過在內皮細胞之間的微小縫隙更容易到達動脈壁內。
The endothelium is a thin layer of cells which covers the inner wall of the arteries.
內皮是薄層細胞覆蓋在動脈的內壁。
The cells making up the endothelium have tiny gaps between them.
組成內皮的細胞之間有微小的差距。
Others postulate that the smaller LDL cholesterol particles are more easily oxidized.
其他研究推測較小LDL膽固醇顆粒更容易被氧化。
Oxidation of cholesterol is significant in the formation of cholesterol plaques.
膽固醇的氧化是會導致膽固醇斑塊顯著的形成。
How can LDL cholesterol size be enlarged?
如何能將LDL膽固醇的尺寸放大？
Even though LDL cholesterol particle size is mainly genetically inherited, individuals who have small LDL particles (pattern B) can increase their particle size through diet, exercise, and medications.
儘管LDL膽固醇粒徑尺寸主要是來自於基因遺傳，但是擁有小LDL顆粒（模式B）的個體可以通過飲食、鍛煉和藥物治療來增加顆粒尺寸。
Diets that are low in saturated fat and cholesterol, regular aerobic exercise, and loss of excess body fat have been determined to decrease the number of small LDL particles and increase the number of large LDL particles in the blood.
含有較少飽和脂肪和膽固醇的飲食、規律的有氧運動、和減少體內多餘的脂肪可以降低小LDL顆粒的數量，並提高在血液中的大LDL顆粒的數量。
In other words, lifestyle modifications can change pattern B to pattern A.
換句話說，生活方式的改變可以將模式B切換到模式A。
When lifestyle changes alone are unsuccessful, medications can be used.
當只靠改變生活的方式無效時，可以採用藥物治療。
Even though the statin medications (discussed above) are effective in lowering the absolute levels of LDL cholesterol, they appear to have a limited effect on LDL cholesterol size pattern.
即使他汀類藥物能有效地降低LDL膽固醇的絕對水平，它們對特定尺寸的LDL膽固醇顆粒效果有限。
Medications such as nicotinic acid (niacin) and gemfibrozil (Lopid) have been found effective in many instances in increasing the size of LDL cholesterol particles.
如菸酸（菸酸）和吉非貝齊（Lopid）等藥物已經在許多情況下被發現能有效的增加的LDL膽固醇的顆粒的大小。
Lipoprotein (a) (Lp(a)) is an LDL cholesterol particle that is attached to a special protein called apo(a). In large part, a person’s level of Lp(a) in the blood is genetically inherited.
Lp(a)是一種LDL膽固醇顆粒，附著在一種特殊蛋白質稱為Apo(a)。在很大程度上，一個人血液中的Lp(a)是來自基因遺傳。
Lipoprotein (a) (Lp(a)) is an LDL cholesterol particle that is attached to a special protein called apo(a). In large part, a person’s level of Lp(a) in the blood is genetically inherited.
Lp(a)是一種LDL膽固醇顆粒，附著在一種特殊蛋白質稱為Apo(a)。在很大程度上，一個人血液中的Lp(a)是來自基因遺傳。
Lipoprotein (a) (Lp(a)) is an LDL cholesterol particle that is attached to a special protein called apo(a). In large part, a person’s level of Lp(a) in the blood is genetically inherited.
Lp(a)是一種LDL膽固醇顆粒，附著在一種特殊蛋白質稱為Apo(a)。在很大程度上，一個人血液中的Lp(a)是來自基因遺傳。
Elevated levels of Lp(a) (higher than 20 mg/dl to 30 mg/dl) in the blood are linked to a greater likelihood of atherosclerosis and heart attacks in both men and women.
在男性和女性，血液中的Lp(a) 水平升高（高於20~30毫克/分升）與動脈粥樣硬化和心臟病發作的風險增加有關。
The risk is even more significant if the Lp(a) cholesterol elevation is accompanied by high LDL/HDL ratios.
如果Lp(a)膽固醇升高伴隨高LDL/ HDL比率時風險更顯著。
Certain diseases are associated with elevated Lp(a) levels. Patients on chronic kidney dialysis and those with nephrotic syndromes (kidney diseases that cause leakage of blood proteins into the urine) tend to have high levels of Lp(a).
某些疾病與升高的Lp（a）水平相關聯。對於慢性腎透析和腎病綜合症（腎臟疾病，導致血液中的蛋白質滲漏進入尿液）的患者通常具有高含量的Lp（a）。
There are many theories as to how Lp(a) causes atherosclerosis although exactly how Lp(a) accumulates cholesterol plaques on the artery walls has not been well defined.
目前有很多理論來說明Lp(a)如何導致動脈粥樣硬化，但是究竟Lp(a)是如何在動脈壁累積膽固醇斑塊尚未明確。
Clinical trials conclusively proving that lowering Lp(a) reduces atherosclerosis and the risk of heart attacks have not been conducted.
證明降低Lp(a)可以減少動脈粥樣硬化和心臟病發作風險的臨床試驗尚未進行。
Currently, there is no international standard for determining Lp(a) cholesterol levels and commercial sources of Lp(a) testing may not have the same accuracy as research laboratories.
目前，還沒有一個決定Lp(a) 膽固醇水平的國際標準，而且測試Lp(a)的商業機構無法達到研究實驗室相同的精度。
Therefore, specifically measuring and treating elevated Lp(a) cholesterol levels are not widely performed in this country.
因此，對於升高的Lp(a) 膽固醇水平還沒有具體的測量和治療被廣泛的進行。
How can Lp(a) cholesterol levels be reduced?
如何降低Lp(a) 膽固醇水平?
Most lipid-lowering medications such as statins, Lopid, and cholestyramine have a limited effect in lowering Lp(a) cholesterol levels.
大部分降脂藥物如他汀類，Lopid，和烯胺在降低Lp(a)膽固醇水平的影響有限。
Estrogen has been shown to lower Lp(a) cholesterol levels by approximately 20% in women with elevated Lp(a) cholesterol.
雌激素已被證明在具有升高Lp(a)膽固醇水平的婦女，可以降低約20％Lp(a)膽固醇水平。
Estrogen can also increase HDL cholesterol levels when given to postmenopausal women.
雌激素對於絕經後的婦女還可以增加HDL膽固醇水平。
Additionally, nicotinic acid (Niacin or Niaspan) in high doses has been found to be effective in lowering Lp(a) cholesterol levels by approximately 30%.
此外，在高劑量的菸酸（Niacin或Niaspan）已被證明可以有效的降低Lp(a)膽固醇水平約30％。
極低密度脂蛋白（VLDL）將（新合成的）甘油三酯從肝臟帶往脂肪組織。
HDL is the lipoprotein transporting cholesterol from the tissues back to the liver for excretion into bile for elimination in the bowel but in the small bowel 70% of cholesterol excreted ultimately is reincorporated with diet fat into chylomicrons in the enterocyte to begin the whole process again.
HDL是將膽固醇從組織運回到肝臟，並排泄進入膽汁在腸道中進行消除，但在小腸中70％的膽固醇最終與經由飲食所吸收的脂肪組在腸上皮細胞中組成乳糜微粒中重新開始整個運輸的過程。
HDL is the lipoprotein transporting cholesterol from the tissues back to the liver for excretion into bile for elimination in the bowel but in the small bowel 70% of cholesterol excreted ultimately is reincorporated with diet fat into chylomicrons in the enterocyte to begin the whole process again.
HDL是將膽固醇從組織運回到肝臟，並排泄進入膽汁在腸道中進行消除，但在小腸中70％的膽固醇最終與經由飲食所吸收的脂肪組在腸上皮細胞中組成乳糜微粒中重新開始整個運輸的過程。
HDL is synthesized by the liver cells (and other gastro intestinal cells) and is a unique lipoprotein containing one integral transmembrane apoA apoprotein.
HDL是由肝細胞（和其他胃腸細胞）所合成的，含有一個整合形跨膜載脂蛋白Apo A。
HDL when synthesized has very little triglyceride or free cholesterol and is essentially “empty” as its job is to acquire cholesterol from the periphery to transport back to the liver.
HDL合成初期具有非常小量的甘油三酯或游離膽固醇，實質上是“空”的它的工作是從外圍組織獲得膽固醇輸並送回肝臟。
HDL when synthesized has very little triglyceride or free cholesterol and is essentially “empty” as its job is to acquire cholesterol from the periphery to transport back to the liver.
HDL合成初期具有非常小量的甘油三酯或游離膽固醇，實質上是“空”的它的工作是從外圍組織獲得膽固醇輸並送回肝臟。
In the circulation the empty HDL acquires an enzyme LCAT (lecithin-cholesterol-acyl transferase).
在循環的過程中HDL獲得一種酶（lecithin-cholesterol-acyl transferase, LCAT）卵磷脂膽固醇酰基轉移）。卵磷脂-膽固醇脂醯基轉移酶
LCAT:lecithin cholesterol acyltransferase 卵磷脂膽固醇乙醯基轉移酶（催化膽固醇脂化）
The HDL with LCAT imbedded in its monolayer membrane attaches to any cell binding to the cholesterol esters in the outer layer of the phospholipid bilayer cell membranes and the LCAT attaches to the Hydroxy group on the cholesterol ester and extracts the ester from the outer cell membrane into the HDL molecule.
LCAT嵌入於HDL的單層膜上，HDL附著到任何細胞中的磷脂雙層細胞膜外層的膽固醇酯，LCAT附著在膽固醇酯的羥基基團，並從外細胞膜提取膽固醇酯進入HDL。
Thus HDL takes cholesterol from peripheral cells and loads the cholesterol ester into the HDL and transports this back to the liver attaching to the apoA-receptor on the liver cell for the cholesterol to be synthesized in bile.
所以HDL從週邊細胞吸收膽固醇，並裝載膽固醇酯進入HDL核心，藉由肝細胞的Apo A受體運輸回到肝臟，將膽固醇用於膽汁的合成。
So in deficient HDL (low HDL) states there is less of this carrier molecule to unload the cells and arterial wall of cholesterol content hence an independent risk for vascular disease.
因此，在缺乏高密度脂蛋白（HDL低）狀態有較少這種載體分子卸載細胞和膽固醇含量，因此血管疾病的獨立危險動脈壁。
Like LDL you can equally understand the MISNOMER of HDL being “good cholesterol” as low levels potentiate vascular disease whilst high HDL tends to protect against atherosclerosis BUT it is NOT cholesterol that is implicated; it is the carrier molecule HDL.
就像LDL可以理解同樣是高密度脂蛋白“好膽固醇”的水平低使可能血管疾病，而高密度脂蛋白趨於防止動脈粥樣硬化，但它是不是有牽連膽固醇的用詞不當;它是載體分子HDL。
Much has been made of the “reverse cholesterol transport” mechanism whereby HDL extracts cholesterol from arterial plaques, but HDL has other importance roles in atherosclerosis with its antioxidant and anti-inflammatory properties key to the protective effect of HDL.
雖然HDL經由“反向膽固醇運輸”機制已經從動脈斑塊中提取膽固醇，但是HDL因其抗氧化和抗炎性質的關鍵保護特性，所以在動脈粥樣硬化上扮演重要的作用。
