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Hypertriglyceridemic HyperapoB: The Unappreciated Atherogenic Dyslipoproteinemia in Type 2 Diabetes Mellitus

Allan D. Sniderman, MD; Thea Scantlebury, BSc; and Katherine Cianflone, PhD
[+] Article and Author Information

From McGill University Health Centre, McGill University, and Concordia University, Montreal, Quebec, Canada.


Acknowledgments: The authors thank Dr. J. Wiseman, an academic clinical internist, for encouragement and support.

Grant Support: By grant MT-5480 from the Medical Research Council of Canada (Dr. Sniderman). Ms. Scantlebury is a recipient of the Medical Research Council of Canada Doctoral Research Award (9810DRN-1414-58633). Dr. Cianflone is a recipient of a scholarship from the Fonds de la Recherche en Santé du Québec.

Requests for Single Reprints: Allan D. Sniderman, MD, Mike Rosenbloom Laboratory for Cardiovascular Research, Room H7.22, McGill University Health Centre, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada; e-mail, allan.sniderman@muhc.mcgill.ca.

Current Author Addresses: Dr. Sniderman: Mike Rosenbloom Laboratory for Cardiovascular Research, Room H7.22, McGill University Health Centre, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada.

Ms. Scantlebury and Dr. Cianflone: Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada.


Ann Intern Med. 2001;135(6):447-459. doi:10.7326/0003-4819-135-6-200109180-00014
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Worldwide, more than 100 million people have type 2 diabetes mellitus, and that number will more than double in the next 10 years (1). Of these persons, more than three of four—that is, more than 150 million people—are expected to die of cardiovascular disease over the next decade (2). A history of diabetes is equivalent in risk for death to a history of myocardial infarction, and the combination compounds the risk (3).

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Figures

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Figure 1.
Differences between lipoprotein lipids and lipoprotein particles in a patient with a plasma triglyceride level of 3 mmol/L (264 mg/dL) and a low-density lipoprotein (LDL) cholesterol level of 3 mmol/L (116 mg/dL).

B = apoB100; CE = cholesterol ester; Tg = triglyceride.

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Figure 2.
The relative number of very-low-density lipoprotein (VLDL) (left), intermediate-density lipoprotein (middle), and low-density lipoprotein (LDL) (right) particles.

The LDL particles always greatly outnumber VLDL particles. The LDL particles also differ in composition; in this instance, most LDL particles are LDL A rather than LDL B. B = apoB100; CE = cholesterol ester; Tg = triglyceride.

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Figure 3.
Formation of small, dense low-density lipoprotein (LDL) particles.CETPLPLHL

Two steps are involved in the formation of small, dense LDL particles. The first is lipid transfer mediated by cholesterol ester transfer protein ( ); the second is lipid hydrolysis by lipoprotein lipase ( ) and hepatic lipase ( ). B = apoB100; CE = cholesterol ester; Tg = triglyceride; VLDL = very-low-density lipoprotein.

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Grahic Jump Location
Figure 4.
ApoB lipoprotein particles in healthy persons (left) and those with hypertriglyceridemic hyperapoB (right).

B = apoB100; CE = cholesterol ester; LDL = low-density lipoprotein; Tg = triglycerides.

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