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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1314.)
© 2003 American Heart Association, Inc.

Editorials

Cholesterol Absorption and the Metabolic Syndrome

A New Look at an Old Area

Lars Berglund; Dianne Hyson

Department of Medicine (L.B.), University of California Davis, Davis; and Family and Consumer Sciences Department (D.H.), California State University, Sacramento.

Correspondence to Lars Berglund, MD, Department of Medicine, University of California Davis, UCD Medical Center, 4150 V St, Ste G400, Sacramento, CA 95817. E-mail lberglund@ucdavis.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The metabolic syndrome is recognized as an important risk factor for atherosclerosis and much attention has focused on its treatment.¹ The dyslipidemia pattern in this syndrome is characterized by increased triglyceride levels, low HDL cholesterol levels, and a qualitative and sometimes quantitative change in LDL cholesterol levels.² Although underlying mechanisms for this pattern are not fully understood, it is believed that insulin resistance resulting in an increased flow of free fatty acids from adipose tissue to the liver is a major contributor. The increased availability of fatty acids for triglyceride formation is a driving force for increased hepatic secretion of triglyceride-rich lipoproteins with secondary effects on HDL and LDL metabolism.^2,3 Under normolipidemic conditions in humans, VLDL secretion is affected by triglyceride and cholesterol availability, and recent studies suggest an association between cholesterol synthesis and production of smaller VLDL particles (VLDL-2).^4,5 While insulin suppresses the formation of large VLDL particles, it does not impact the production of the smaller VLDL-2 fraction.⁶

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Dietary modification with a reduction of saturated fat and cholesterol as well as focus on overall caloric intake is the foundation for treatment of dyslipidemia.⁷ The relationship between dietary fat intake and cholesterol absorption is well established, and responses to changes in dietary cholesterol are related to dietary saturated fat content.^8–10 Thus, in a recent meta-analysis, a dietary cholesterol challenge of 100 mg from eggs resulted in 70% higher increase in LDL cholesterol on a high versus a low saturated fat diet.¹¹ However, the response in plasma . . . [Full Text of this Article]

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