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IS ATHEROSCLEROSIS EXCLUSIVELY A POSTPRANDIAL PHENOMENON?
SUMMARY 1. Atherosclerosis begins with the deposition of cholesterol in arterial tissue that is thought to be derived from circulating lipoproteins. There is considerable evidence implicating low density lipoprotein (LDL) as a primary source of plaque cholesterol and, consequently, there are many ar...
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| Published in: | Clinical and experimental pharmacology & physiology 1997-04, Vol.24 (3-4), p.288-293 |
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| Main Authors: | , , , , , , , |
| Format: | Article |
| Language: | English |
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| container_end_page | 293 |
| container_issue | 3-4 |
| container_start_page | 288 |
| container_title | Clinical and experimental pharmacology & physiology |
| container_volume | 24 |
| creator | Mamo, John CL Yu, Kenneth CW Elsegood, Caryn L. Smith, Darrin Vine, Donna Gennat, Hanni C. Voevodin, Melanie Proctor, Spencer D. |
| description | SUMMARY
1. Atherosclerosis begins with the deposition of cholesterol in arterial tissue that is thought to be derived from circulating lipoproteins. There is considerable evidence implicating low density lipoprotein (LDL) as a primary source of plaque cholesterol and, consequently, there are many articles that deal with various aspects of LDL metabolism.
2. Postprandial lipoproteins (i.e. chylomicrons transporting dietary fats) are also considered pro‐atherogenic; however, it is less clear whether their involvement in arterial cholesterol deposition is direct or follows modulation of LDL metabolism.
3. In order to provoke discussion, this article is presented in a manner that suggests atherosclerosis to be exclusively a postprandial phenomenon; that is, we have raised the possibility that LDL is non‐atherogenic. |
| doi_str_mv | 10.1111/j.1440-1681.1997.tb01822.x |
| format | article |
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1. Atherosclerosis begins with the deposition of cholesterol in arterial tissue that is thought to be derived from circulating lipoproteins. There is considerable evidence implicating low density lipoprotein (LDL) as a primary source of plaque cholesterol and, consequently, there are many articles that deal with various aspects of LDL metabolism.
2. Postprandial lipoproteins (i.e. chylomicrons transporting dietary fats) are also considered pro‐atherogenic; however, it is less clear whether their involvement in arterial cholesterol deposition is direct or follows modulation of LDL metabolism.
3. In order to provoke discussion, this article is presented in a manner that suggests atherosclerosis to be exclusively a postprandial phenomenon; that is, we have raised the possibility that LDL is non‐atherogenic.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/j.1440-1681.1997.tb01822.x</identifier><identifier>PMID: 9131300</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Arteriosclerosis - etiology ; Arteriosclerosis - metabolism ; atherosclerosis ; Biological Transport ; chylomicrons ; Chylomicrons - metabolism ; Foam Cells - physiology ; Humans ; Lipoproteins, LDL - metabolism ; low density lipoproteins ; Postprandial Period ; postprandial phenomenon</subject><ispartof>Clinical and experimental pharmacology & physiology, 1997-04, Vol.24 (3-4), p.288-293</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4228-d39b828d54c4f6dd866ece55fe5476a373d8f10e97ff92f0937656fbab936a493</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9131300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mamo, John CL</creatorcontrib><creatorcontrib>Yu, Kenneth CW</creatorcontrib><creatorcontrib>Elsegood, Caryn L.</creatorcontrib><creatorcontrib>Smith, Darrin</creatorcontrib><creatorcontrib>Vine, Donna</creatorcontrib><creatorcontrib>Gennat, Hanni C.</creatorcontrib><creatorcontrib>Voevodin, Melanie</creatorcontrib><creatorcontrib>Proctor, Spencer D.</creatorcontrib><title>IS ATHEROSCLEROSIS EXCLUSIVELY A POSTPRANDIAL PHENOMENON?</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>SUMMARY
1. Atherosclerosis begins with the deposition of cholesterol in arterial tissue that is thought to be derived from circulating lipoproteins. There is considerable evidence implicating low density lipoprotein (LDL) as a primary source of plaque cholesterol and, consequently, there are many articles that deal with various aspects of LDL metabolism.
2. Postprandial lipoproteins (i.e. chylomicrons transporting dietary fats) are also considered pro‐atherogenic; however, it is less clear whether their involvement in arterial cholesterol deposition is direct or follows modulation of LDL metabolism.
3. In order to provoke discussion, this article is presented in a manner that suggests atherosclerosis to be exclusively a postprandial phenomenon; that is, we have raised the possibility that LDL is non‐atherogenic.</description><subject>Animals</subject><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - metabolism</subject><subject>atherosclerosis</subject><subject>Biological Transport</subject><subject>chylomicrons</subject><subject>Chylomicrons - metabolism</subject><subject>Foam Cells - physiology</subject><subject>Humans</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>low density lipoproteins</subject><subject>Postprandial Period</subject><subject>postprandial phenomenon</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNo9kNlqwlAQhg-lxVrbRyiEXvQu6VlytpuWkMYFYiIau1wNWU5Aq9UmSu3bN0FxYGYY_uEf5kPogWCHNPG0dIjrYpsIRRyitXR2GSaKUudwgbpn6RJ1McPcJkria3RT10uMMceCdVBHE0YYxl2kRzPLS4bBNJ75YVubOfjww_ls9BaEn5ZnTeJZMpl60evIC63JMIjicZPRyy26KtNVbe5OvYfm_SDxh3YYD0a-F9q5S6myC6YzRVXB3dwtRVEoIUxuOC8Nd6VImWSFKgk2WpalpiXWTAouyizNNBOpq1kPPR59t9XmZ2_qHawXdW5Wq_TbbPY1SKU55VQ1i_enxX22NgVsq8U6rf7g9GujPx_138XK_J1lgqGFCktoyUFLDlqocIIKB_CDCVXtAftosKh35nA2SKsvEJJJDu_RAEQihEj6Y-DsH9bsdB8</recordid><startdate>199704</startdate><enddate>199704</enddate><creator>Mamo, John CL</creator><creator>Yu, Kenneth CW</creator><creator>Elsegood, Caryn L.</creator><creator>Smith, Darrin</creator><creator>Vine, Donna</creator><creator>Gennat, Hanni C.</creator><creator>Voevodin, Melanie</creator><creator>Proctor, Spencer D.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>199704</creationdate><title>IS ATHEROSCLEROSIS EXCLUSIVELY A POSTPRANDIAL PHENOMENON?</title><author>Mamo, John CL ; Yu, Kenneth CW ; Elsegood, Caryn L. ; Smith, Darrin ; Vine, Donna ; Gennat, Hanni C. ; Voevodin, Melanie ; Proctor, Spencer D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4228-d39b828d54c4f6dd866ece55fe5476a373d8f10e97ff92f0937656fbab936a493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Arteriosclerosis - etiology</topic><topic>Arteriosclerosis - metabolism</topic><topic>atherosclerosis</topic><topic>Biological Transport</topic><topic>chylomicrons</topic><topic>Chylomicrons - metabolism</topic><topic>Foam Cells - physiology</topic><topic>Humans</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>low density lipoproteins</topic><topic>Postprandial Period</topic><topic>postprandial phenomenon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mamo, John CL</creatorcontrib><creatorcontrib>Yu, Kenneth CW</creatorcontrib><creatorcontrib>Elsegood, Caryn L.</creatorcontrib><creatorcontrib>Smith, Darrin</creatorcontrib><creatorcontrib>Vine, Donna</creatorcontrib><creatorcontrib>Gennat, Hanni C.</creatorcontrib><creatorcontrib>Voevodin, Melanie</creatorcontrib><creatorcontrib>Proctor, Spencer D.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental pharmacology & physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mamo, John CL</au><au>Yu, Kenneth CW</au><au>Elsegood, Caryn L.</au><au>Smith, Darrin</au><au>Vine, Donna</au><au>Gennat, Hanni C.</au><au>Voevodin, Melanie</au><au>Proctor, Spencer D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IS ATHEROSCLEROSIS EXCLUSIVELY A POSTPRANDIAL PHENOMENON?</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>1997-04</date><risdate>1997</risdate><volume>24</volume><issue>3-4</issue><spage>288</spage><epage>293</epage><pages>288-293</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>SUMMARY
1. Atherosclerosis begins with the deposition of cholesterol in arterial tissue that is thought to be derived from circulating lipoproteins. There is considerable evidence implicating low density lipoprotein (LDL) as a primary source of plaque cholesterol and, consequently, there are many articles that deal with various aspects of LDL metabolism.
2. Postprandial lipoproteins (i.e. chylomicrons transporting dietary fats) are also considered pro‐atherogenic; however, it is less clear whether their involvement in arterial cholesterol deposition is direct or follows modulation of LDL metabolism.
3. In order to provoke discussion, this article is presented in a manner that suggests atherosclerosis to be exclusively a postprandial phenomenon; that is, we have raised the possibility that LDL is non‐atherogenic.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9131300</pmid><doi>10.1111/j.1440-1681.1997.tb01822.x</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0305-1870 |
| ispartof | Clinical and experimental pharmacology & physiology, 1997-04, Vol.24 (3-4), p.288-293 |
| issn | 0305-1870 1440-1681 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_78952528 |
| source | Wiley |
| subjects | Animals Arteriosclerosis - etiology Arteriosclerosis - metabolism atherosclerosis Biological Transport chylomicrons Chylomicrons - metabolism Foam Cells - physiology Humans Lipoproteins, LDL - metabolism low density lipoproteins Postprandial Period postprandial phenomenon |
| title | IS ATHEROSCLEROSIS EXCLUSIVELY A POSTPRANDIAL PHENOMENON? |
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