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Introduction to Lipids and Lipoproteins.

Authors

Feingold KR22, Grunfeld C23.

Source

Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.
2018 Feb 2.

Author information

1
Professor of Medicine, University of California, San Francisco, CA
2
Chief of Medicine at the University of Washington Medical Center and Professor and Vice Chair of the Department of Medicine, University of Washington
3
Pediatric Endocrinologist and Associate Research Physician in the Skeletal Diseases and Mineral Homeostasis Section, National Institute of Dental and Craniofacial Research, National Institutes of Health
4
Professor of Pediatrics and Endocrinology, Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, "Aghia Sophia" Children's Hospital, Athens, Greece
5
Associate Professor of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Ohio State University
6
Professor of Endocrinology and Director of the Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, UK
7
Distinguished Professor of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA; Associate Chief, Endocrinology and Diabetes Division and Director, Endocrine Clinic, West Los Angeles VA Medical Center, Los Angeles, CA
8
Professor of General Medicine-Endocrinology, First Department of Propaedeutic Internal Medicine, Laiko University Hospital, Athens, Greece
9
Head of the Medicover MVZ Oldenburg; affiliated with the Carl von Ossietzky University and the Technical University of Dresden
10
Professor of Medicine and Chief of the Division of Endocrinology, Diabetology and Metabolism, University of Lausanne, Switzerland
11
Professor of Endocrinology and Metabolism, Centre Lead for Endocrinology and Deputy Institute Director, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, England
12
Director of Clinical Research, Hudson Institute of Medical Research; Consultant Endocrinologist, Monash Medical Centre, Melbourne, Australia
13
Dammert Professor of Gerontology and Director, Division of Geriatric Medicine and Director of the Division of Endocrinology, Saint Louis University Medical Center
14
Professor of Pediatrics, Professor of Genetics and Genomic Sciences, and Chief of the Adrenal Steroid Disorders Program, Icahn School of Medicine, Mount Sinai School of Medicine, New York, NY
15
Associate Professor of Medicine and Epidemiology, University of Colorado Anschutz Medical Campus
16
Professor of Medicine, Knight Cardiovascular Institute and the Division of Endocrinology, and Associate Director, Bob and Charlee Moore Institute for Nutrition and Wellness, Oregon Health and Science University, Portland, OR
17
Professor and Chair, Department of Obstetrics and Gynecology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI
18
Director of the Endocrine/Bone Disease Program, John Wayne Cancer Institute at Saint John’s Health Center, Santa Monica, CA; Clinical Professor of Medicine, UCLA School of Medicine, Los Angeles, CA
19
Director of the Diabetes Care Center and Associate Professor of Medicine, University of Washington Medical Center, Seattle, WA
20
Murray Waitzer Endowed Chair for Diabetes Research, Professor of Medicine/Pathology/Neurobiology, Director of Research and Neuroendocrine Unit Division of Endocrine and Metabolic Disorders, Eastern Virginia Medical School, Norfolk, VA
21
Endowed Chair, Cardiovascular Health and Risk Prevention, Pediatric Endocrinology and Diabetes, Cook Children's Medical Center, Fort Worth, TX
22
Kenneth R. Feingold, MD, received his medical degree from the State University of New York, Upstate Medical Center in Syracuse, New York. He completed his internship and residency in internal medicine at the University of Wisconsin in Madison, Wisconsin and a fellowship in endocrinology and metabolism at the University of California, San Francisco. He is currently a Professor of Medicine in the Endocrinology Section at the University of California San Francisco and a Staff Physician at the San Francisco VA Medical Center. For many years he was Chief of the Endocrine at the San Francisco VA.
23
Professor of Medicine, University of California- San Francisco; Chief of the Metabolism and Endocrine Section and Associate Chief of Staff for Research and Development-San Francisco VA Medical Center, Metabolism 111F, VA Medical Center, 4150 Clement St, San Francisco, CA 94121

Excerpt

Cholesterol and triglycerides are insoluble in water and therefore these lipids must be transported in association with proteins. Lipoproteins are complex particles with a central core containing cholesterol esters and triglycerides surrounded by free cholesterol, phospholipids, and apolipoproteins, which facilitate lipoprotein formation and function. Plasma lipoproteins can be divided into seven classes based on size, lipid composition, and apolipoproteins (chylomicrons, chylomicron remnants, VLDL, IDL, LDL, HDL, and Lp (a)). Chylomicron remnants, VLDL, IDL, LDL, and Lp (a) are all pro-atherogenic while HDL is anti-atherogenic. Apolipoproteins have four major functions including 1) serving a structural role, 2) acting as ligands for lipoprotein receptors, 3) guiding the formation of lipoproteins, and 4) serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins. The exogenous lipoprotein pathway starts with the incorporation of dietary lipids into chylomicrons in the intestine. In the circulation, the triglycerides carried in chylomicrons are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids, which are subsequently metabolized by muscle and adipose tissue, and chylomicron remnants are formed. Chylomicron remnants are then taken up by the liver. The endogenous lipoprotein pathway begins in the liver with the formation of VLDL. The triglycerides carried in VLDL are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids and IDL are formed. The IDL are further metabolized to LDL, which are taken up by via the LDL receptor in numerous tissues including the liver, the predominant site of uptake. Reverse cholesterol transport begins with the formation of nascent HDL by the liver and intestine. These small HDL particles can then acquire cholesterol and phospholipids that are effluxed from cells, a process mediated by ABCA1 resulting in the formation of mature HDL. Mature HDL can acquire addition cholesterol from cells via ABCG1, SR-B1, or passive diffusion. The HDL then transports the cholesterol to the liver either directly by interacting with hepatic SR-B1 or indirectly by transferring the cholesterol to VLDL or LDL, a process facilitated by CETP. Cholesterol efflux from macrophages to HDL plays an important role in protecting from the development of atherosclerosis. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

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