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Apolipoprotein A5 and Hypertriglyceridemia

¹ Division of Cardiovascular Medicine, Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, United Kingdom

^aAuthor for correspondence.

The first 20% of the full text of this article appears below.

Hypertriglyceridemia is associated with increased risk of coronary heart disease (CHD) (1)(2)(3)(4)(5), and it is an integral component of the overlapping syndromes of familial combined hyperlipidemia, insulin resistance syndrome, atherogenic lipoprotein profile, and hyperapobetalipoproteinemia (6). More than one mechanism may be involved in the increased risk of CHD associated with increased serum triglycerides:

• Triglyceride-rich lipoproteins (TGRLs) may participate directly in atherogenesis, particularly when they have undergone attack by oxygen free radicals (7).
  
• TGRLs may decrease circulating concentrations of HDL-cholesterol by attracting cholesteryl ester out of HDL in a process mediated by cholesteryl ester transfer protein (CETP). Furthermore, cholesteryl ester, which might otherwise undergo uptake by the hepatic scavenger receptor B1 receptor and thus complete reverse cholesterol transport, can be redirected into chylomicrons and VLDL by CETP. From chylomicrons and VLDL in the circulation, the triglycerides can enter chylomicron remnants and LDL (derived from chylomicrons and VLDL, respectively), both of which are atherogenic (8).
  
• Increased circulating concentrations of TGRLs are also intimately associated with the formation of small, dense LDL (9). This small, cholesterol-depleted LDL subspecies is particularly atherogenic and is the cause of the increase in serum apolipoprotein B (apo B) in hyperapobetalipoproteinemia, which is disproportionately greater than the increase in LDL-cholesterol (10).
  

The most common reason for an increase in circulating triglycerides is increased hepatic secretion of VLDL (11)(12)(. . . [Full Text of this Article]

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