Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy
Genetic linkage studies implicated deficiency of CD36, a membrane fatty acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of the spontaneously hypertensive rat (SHR). In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phen...
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Veröffentlicht in: | The Journal of biological chemistry 2001-06, Vol.276 (26), p.23661-23666 |
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creator | Hajri, Tahar Ibrahimi, Azeddine Coburn, Chris T. Knapp, F.F. Kurtz, Ted Pravenec, Michael Abumrad, Nada A. |
description | Genetic linkage studies implicated deficiency of CD36, a membrane fatty acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of the spontaneously hypertensive rat (SHR). In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized β-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its intravenous injection. Fatty acid transport was also measured in vitro over 20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and from a congenic line (SHRchr4) that incorporates a piece of chromosome 4 containing wild-type CD36. SHR heart and adipose tissue exhibited defects in FA uptake and in conversion of diglycerides to triglycerides that are similar to those observed in the CD36 null mouse. However, a key difference in SHR tissues is that fatty acid oxidation is much more severely impaired than fatty acid esterification, which may underlie the 4–5-fold accumulation of free BMIPP measured in SHR muscle. Studies with isolated adipocytes and cardiomyocytes directly confirmed both the defect in FA transport and the fact that it is underestimated by BMIPP. Heart, oxidative muscle, and adipose tissue in the SHR exhibited a large increase in glucose uptake measured in vivo using [18F]fluorodeoxyglucose. Supplementation of the diet with short-chain fatty acids, which do not require CD36-facilitated transport, eliminated the increase in glucose uptake, the hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that lack of metabolic energy consequent to deficient FA uptake is the primary defect responsible for these abnormalities. Hypertension was not alleviated by the supplemented diet suggesting it is unrelated to fuel supply and any contribution of CD36 deficiency to this trait may be more complex to determine. It may be worth exploring whether short-chain FA supplementation can reverse some of the deleterious effects of CD36 deficiency in humans, which may include hypertrophic cardiomyopathy. |
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In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized β-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its intravenous injection. Fatty acid transport was also measured in vitro over 20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and from a congenic line (SHRchr4) that incorporates a piece of chromosome 4 containing wild-type CD36. SHR heart and adipose tissue exhibited defects in FA uptake and in conversion of diglycerides to triglycerides that are similar to those observed in the CD36 null mouse. However, a key difference in SHR tissues is that fatty acid oxidation is much more severely impaired than fatty acid esterification, which may underlie the 4–5-fold accumulation of free BMIPP measured in SHR muscle. Studies with isolated adipocytes and cardiomyocytes directly confirmed both the defect in FA transport and the fact that it is underestimated by BMIPP. Heart, oxidative muscle, and adipose tissue in the SHR exhibited a large increase in glucose uptake measured in vivo using [18F]fluorodeoxyglucose. Supplementation of the diet with short-chain fatty acids, which do not require CD36-facilitated transport, eliminated the increase in glucose uptake, the hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that lack of metabolic energy consequent to deficient FA uptake is the primary defect responsible for these abnormalities. Hypertension was not alleviated by the supplemented diet suggesting it is unrelated to fuel supply and any contribution of CD36 deficiency to this trait may be more complex to determine. It may be worth exploring whether short-chain FA supplementation can reverse some of the deleterious effects of CD36 deficiency in humans, which may include hypertrophic cardiomyopathy.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M100942200</identifier><identifier>PMID: 11323420</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adipose Tissue - metabolism ; Animals ; Animals, Congenic ; b-methyliodophenyl pentadecanoic acid ; Biological Transport ; Cardiomegaly - etiology ; Cardiomegaly - metabolism ; CD36 Antigens - genetics ; CD36 Antigens - metabolism ; CD36 protein ; Cells, Cultured ; chromosome 4 ; Fatty Acids - metabolism ; Fluorodeoxyglucose F18 - metabolism ; Glucose - metabolism ; Glucose Tolerance Test ; hyperinsulinemia ; Hyperinsulinism - etiology ; Hyperinsulinism - metabolism ; Hypertension - complications ; Iodobenzenes - metabolism ; Myocardium - metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Tissue Distribution</subject><ispartof>The Journal of biological chemistry, 2001-06, Vol.276 (26), p.23661-23666</ispartof><rights>2001 © 2001 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-e28293abd0c39029ce12cb64c854a836cb50c38eb19a41937e12f3aba85ebe03</citedby><cites>FETCH-LOGICAL-c506t-e28293abd0c39029ce12cb64c854a836cb50c38eb19a41937e12f3aba85ebe03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11323420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hajri, Tahar</creatorcontrib><creatorcontrib>Ibrahimi, Azeddine</creatorcontrib><creatorcontrib>Coburn, Chris T.</creatorcontrib><creatorcontrib>Knapp, F.F.</creatorcontrib><creatorcontrib>Kurtz, Ted</creatorcontrib><creatorcontrib>Pravenec, Michael</creatorcontrib><creatorcontrib>Abumrad, Nada A.</creatorcontrib><title>Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Genetic linkage studies implicated deficiency of CD36, a membrane fatty acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of the spontaneously hypertensive rat (SHR). In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized β-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its intravenous injection. Fatty acid transport was also measured in vitro over 20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and from a congenic line (SHRchr4) that incorporates a piece of chromosome 4 containing wild-type CD36. SHR heart and adipose tissue exhibited defects in FA uptake and in conversion of diglycerides to triglycerides that are similar to those observed in the CD36 null mouse. However, a key difference in SHR tissues is that fatty acid oxidation is much more severely impaired than fatty acid esterification, which may underlie the 4–5-fold accumulation of free BMIPP measured in SHR muscle. Studies with isolated adipocytes and cardiomyocytes directly confirmed both the defect in FA transport and the fact that it is underestimated by BMIPP. Heart, oxidative muscle, and adipose tissue in the SHR exhibited a large increase in glucose uptake measured in vivo using [18F]fluorodeoxyglucose. Supplementation of the diet with short-chain fatty acids, which do not require CD36-facilitated transport, eliminated the increase in glucose uptake, the hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that lack of metabolic energy consequent to deficient FA uptake is the primary defect responsible for these abnormalities. Hypertension was not alleviated by the supplemented diet suggesting it is unrelated to fuel supply and any contribution of CD36 deficiency to this trait may be more complex to determine. It may be worth exploring whether short-chain FA supplementation can reverse some of the deleterious effects of CD36 deficiency in humans, which may include hypertrophic cardiomyopathy.</description><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Animals, Congenic</subject><subject>b-methyliodophenyl pentadecanoic acid</subject><subject>Biological Transport</subject><subject>Cardiomegaly - etiology</subject><subject>Cardiomegaly - metabolism</subject><subject>CD36 Antigens - genetics</subject><subject>CD36 Antigens - metabolism</subject><subject>CD36 protein</subject><subject>Cells, Cultured</subject><subject>chromosome 4</subject><subject>Fatty Acids - metabolism</subject><subject>Fluorodeoxyglucose F18 - metabolism</subject><subject>Glucose - metabolism</subject><subject>Glucose Tolerance Test</subject><subject>hyperinsulinemia</subject><subject>Hyperinsulinism - etiology</subject><subject>Hyperinsulinism - metabolism</subject><subject>Hypertension - complications</subject><subject>Iodobenzenes - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Tissue Distribution</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtv1DAUhS0EokNhyxJ5gVg1gx95Lkd9Sx0VQZHYWbZzQ1wSO9hOq_whfieuMlJXtSxZ1v3OufY9CH2kZEtJlX-9V3q7p4Q0OWOEvEIbSmqe8YL-eo02hDCaNayoj9C7EO5JWnlD36IjSjnjOSMb9O8MOtDRPAC-kDEueKdNi39OUf4BbCyOPeAfk7NRWnBzGBZ8tUzgI9jwpPkuI74OWOJv3ozSL_gMIvjRWGkjdh3eDekKLb4cZu0C4D1EqdxgwniyGhkb5sFYGI08wdK2eL84LX1r5HDo5N3UL-_Rm04OAT4czmN0d3F-d3qV3dxeXp_ubjJdkDJmwGrWcKlaonlDWKOBMq3KXNdFLmtealWkSg2KNjKnDa9SvUu8rAtQQPgx-rLaTt79nSFEMZqgYRjW3wta1U1R5WUCtyuovQvBQyemdQCCEvEUjEjBiOdgkuDTwXlWI7TP-CGJBHxegd787h-NB6GM0z2MglWlYGnzsqQJq1cM0hQeDHgRtAGroU0SHUXrzEtP-A-Ddasv</recordid><startdate>20010629</startdate><enddate>20010629</enddate><creator>Hajri, Tahar</creator><creator>Ibrahimi, Azeddine</creator><creator>Coburn, Chris T.</creator><creator>Knapp, F.F.</creator><creator>Kurtz, Ted</creator><creator>Pravenec, Michael</creator><creator>Abumrad, Nada A.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20010629</creationdate><title>Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy</title><author>Hajri, Tahar ; Ibrahimi, Azeddine ; Coburn, Chris T. ; Knapp, F.F. ; Kurtz, Ted ; Pravenec, Michael ; Abumrad, Nada A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-e28293abd0c39029ce12cb64c854a836cb50c38eb19a41937e12f3aba85ebe03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>Animals, Congenic</topic><topic>b-methyliodophenyl pentadecanoic acid</topic><topic>Biological Transport</topic><topic>Cardiomegaly - etiology</topic><topic>Cardiomegaly - metabolism</topic><topic>CD36 Antigens - genetics</topic><topic>CD36 Antigens - metabolism</topic><topic>CD36 protein</topic><topic>Cells, Cultured</topic><topic>chromosome 4</topic><topic>Fatty Acids - metabolism</topic><topic>Fluorodeoxyglucose F18 - metabolism</topic><topic>Glucose - metabolism</topic><topic>Glucose Tolerance Test</topic><topic>hyperinsulinemia</topic><topic>Hyperinsulinism - etiology</topic><topic>Hyperinsulinism - metabolism</topic><topic>Hypertension - complications</topic><topic>Iodobenzenes - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hajri, Tahar</creatorcontrib><creatorcontrib>Ibrahimi, Azeddine</creatorcontrib><creatorcontrib>Coburn, Chris T.</creatorcontrib><creatorcontrib>Knapp, F.F.</creatorcontrib><creatorcontrib>Kurtz, Ted</creatorcontrib><creatorcontrib>Pravenec, Michael</creatorcontrib><creatorcontrib>Abumrad, Nada A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hajri, Tahar</au><au>Ibrahimi, Azeddine</au><au>Coburn, Chris T.</au><au>Knapp, F.F.</au><au>Kurtz, Ted</au><au>Pravenec, Michael</au><au>Abumrad, Nada A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2001-06-29</date><risdate>2001</risdate><volume>276</volume><issue>26</issue><spage>23661</spage><epage>23666</epage><pages>23661-23666</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Genetic linkage studies implicated deficiency of CD36, a membrane fatty acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of the spontaneously hypertensive rat (SHR). In this study we determined whether loss of CD36 function in FA uptake is a primary determinant of the SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized β-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its intravenous injection. Fatty acid transport was also measured in vitro over 20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and from a congenic line (SHRchr4) that incorporates a piece of chromosome 4 containing wild-type CD36. SHR heart and adipose tissue exhibited defects in FA uptake and in conversion of diglycerides to triglycerides that are similar to those observed in the CD36 null mouse. However, a key difference in SHR tissues is that fatty acid oxidation is much more severely impaired than fatty acid esterification, which may underlie the 4–5-fold accumulation of free BMIPP measured in SHR muscle. Studies with isolated adipocytes and cardiomyocytes directly confirmed both the defect in FA transport and the fact that it is underestimated by BMIPP. Heart, oxidative muscle, and adipose tissue in the SHR exhibited a large increase in glucose uptake measured in vivo using [18F]fluorodeoxyglucose. Supplementation of the diet with short-chain fatty acids, which do not require CD36-facilitated transport, eliminated the increase in glucose uptake, the hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that lack of metabolic energy consequent to deficient FA uptake is the primary defect responsible for these abnormalities. Hypertension was not alleviated by the supplemented diet suggesting it is unrelated to fuel supply and any contribution of CD36 deficiency to this trait may be more complex to determine. It may be worth exploring whether short-chain FA supplementation can reverse some of the deleterious effects of CD36 deficiency in humans, which may include hypertrophic cardiomyopathy.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11323420</pmid><doi>10.1074/jbc.M100942200</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipose Tissue - metabolism Animals Animals, Congenic b-methyliodophenyl pentadecanoic acid Biological Transport Cardiomegaly - etiology Cardiomegaly - metabolism CD36 Antigens - genetics CD36 Antigens - metabolism CD36 protein Cells, Cultured chromosome 4 Fatty Acids - metabolism Fluorodeoxyglucose F18 - metabolism Glucose - metabolism Glucose Tolerance Test hyperinsulinemia Hyperinsulinism - etiology Hyperinsulinism - metabolism Hypertension - complications Iodobenzenes - metabolism Myocardium - metabolism Rats Rats, Inbred SHR Rats, Inbred WKY Tissue Distribution |
title | Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and Myocardial Hypertrophy |
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