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Early alterations in the postprandial VLDL1 apoB‐100 and apoB‐48 metabolism in men with strong heredity for type 2 diabetes

. Objectives.  To study the postprandial triglyceride‐rich lipoprotein (TRL) metabolism, specifically the concentrations of very low‐density lipoproteins (VLDL); from intestine (apoB‐48) and liver (apoB‐100), in men with normal fasting triglycerides but at increased risk of developing type 2 diabete...

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Published in:Journal of internal medicine 2004-02, Vol.255 (2), p.273-279
Main Authors: Johanson, E. H., Jansson, P.‐A., Gustafson, B., Lönn, L., Smith, U., Taskinen, M.‐R., Axelsen, M.
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container_title Journal of internal medicine
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description . Objectives.  To study the postprandial triglyceride‐rich lipoprotein (TRL) metabolism, specifically the concentrations of very low‐density lipoproteins (VLDL); from intestine (apoB‐48) and liver (apoB‐100), in men with normal fasting triglycerides but at increased risk of developing type 2 diabetes. Design.  Cross‐sectional study. Subjects and settings.  Sixteen healthy men with at least two first‐degree relatives with type 2 diabetes were individually matched with 16 control subjects without known diabetes heredity for: age, body mass index, and fasting triglyceride level. They underwent an 8‐h meal tolerance test (919 kcal, 51 g fat) during which lipoproteins were separated by density gradient ultracentrifugation. They were characterized by euglycaemic hyperinsulinaemic clamp, peak VO2, 7‐day diet registration and computed tomography. Results.  The relatives were, as expected, more insulin resistant than the controls and had increased concentration of postprandial VLDL1 particles (49% higher for VLDL1 apoB‐48, P = 0.04 and 21% higher for VLDL1 apoB‐100, P = 0.048). The elevation was related to insulin sensitivity, but not to lifestyle and body composition. Moreover, the concentration of postprandial triglycerides in VLDL1 fraction was inversely related to low‐density lipoprotein (LDL) size in both relatives (rs = −0.60, P = 0.03) and controls (rs = −0.72, P = 0.004). There were no differences in the concentration of triglycerides or apoB‐48 and apoB‐100 particles in the other fractions (plasma, chylomicron or VLDL2). Conclusion.  Increased postprandial concentration of TRLs in the VLDL1 fraction seems to be present at an early stage in the development of diabetes and probably contributes to the excess risk of future coronary events in insulin‐resistant men.
doi_str_mv 10.1046/j.1365-2796.2003.01281.x
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H. ; Jansson, P.‐A. ; Gustafson, B. ; Lönn, L. ; Smith, U. ; Taskinen, M.‐R. ; Axelsen, M.</creator><creatorcontrib>Johanson, E. H. ; Jansson, P.‐A. ; Gustafson, B. ; Lönn, L. ; Smith, U. ; Taskinen, M.‐R. ; Axelsen, M.</creatorcontrib><description>. Objectives.  To study the postprandial triglyceride‐rich lipoprotein (TRL) metabolism, specifically the concentrations of very low‐density lipoproteins (VLDL); from intestine (apoB‐48) and liver (apoB‐100), in men with normal fasting triglycerides but at increased risk of developing type 2 diabetes. Design.  Cross‐sectional study. Subjects and settings.  Sixteen healthy men with at least two first‐degree relatives with type 2 diabetes were individually matched with 16 control subjects without known diabetes heredity for: age, body mass index, and fasting triglyceride level. They underwent an 8‐h meal tolerance test (919 kcal, 51 g fat) during which lipoproteins were separated by density gradient ultracentrifugation. They were characterized by euglycaemic hyperinsulinaemic clamp, peak VO2, 7‐day diet registration and computed tomography. Results.  The relatives were, as expected, more insulin resistant than the controls and had increased concentration of postprandial VLDL1 particles (49% higher for VLDL1 apoB‐48, P = 0.04 and 21% higher for VLDL1 apoB‐100, P = 0.048). The elevation was related to insulin sensitivity, but not to lifestyle and body composition. Moreover, the concentration of postprandial triglycerides in VLDL1 fraction was inversely related to low‐density lipoprotein (LDL) size in both relatives (rs = −0.60, P = 0.03) and controls (rs = −0.72, P = 0.004). There were no differences in the concentration of triglycerides or apoB‐48 and apoB‐100 particles in the other fractions (plasma, chylomicron or VLDL2). Conclusion.  Increased postprandial concentration of TRLs in the VLDL1 fraction seems to be present at an early stage in the development of diabetes and probably contributes to the excess risk of future coronary events in insulin‐resistant men.</description><identifier>ISSN: 0954-6820</identifier><identifier>EISSN: 1365-2796</identifier><identifier>DOI: 10.1046/j.1365-2796.2003.01281.x</identifier><identifier>PMID: 14746565</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adult ; Anthropometry ; Apolipoprotein B-100 ; Apolipoprotein B-48 ; Apolipoproteins B - blood ; apoproteins ; Biological and medical sciences ; Blood Glucose - metabolism ; Cholesterol ; Cholesterol, VLDL - blood ; Cross-Sectional Studies ; Diabetes Mellitus ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; General aspects ; Genetic Predisposition to Disease ; Glucose Tolerance Test ; Humans ; Insulin - blood ; Insulin Resistance ; Life Style ; Male ; MEDICAL AND HEALTH SCIENCES ; Medical sciences ; MEDICIN OCH HÄLSOVETENSKAP ; Middle Aged ; Postprandial Period - physiology ; post‐prandial ; Triglycerides - blood ; triglyceride‐rich lipoproteins ; Type 2/blood/genetics ; VLDL/blood</subject><ispartof>Journal of internal medicine, 2004-02, Vol.255 (2), p.273-279</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Feb 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5101-58748105c021d25a7eb354f2beab183b606467ce6a70603a3635055f61dee2923</citedby><cites>FETCH-LOGICAL-c5101-58748105c021d25a7eb354f2beab183b606467ce6a70603a3635055f61dee2923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=15522074$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14746565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/50366$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Johanson, E. H.</creatorcontrib><creatorcontrib>Jansson, P.‐A.</creatorcontrib><creatorcontrib>Gustafson, B.</creatorcontrib><creatorcontrib>Lönn, L.</creatorcontrib><creatorcontrib>Smith, U.</creatorcontrib><creatorcontrib>Taskinen, M.‐R.</creatorcontrib><creatorcontrib>Axelsen, M.</creatorcontrib><title>Early alterations in the postprandial VLDL1 apoB‐100 and apoB‐48 metabolism in men with strong heredity for type 2 diabetes</title><title>Journal of internal medicine</title><addtitle>J Intern Med</addtitle><description>. Objectives.  To study the postprandial triglyceride‐rich lipoprotein (TRL) metabolism, specifically the concentrations of very low‐density lipoproteins (VLDL); from intestine (apoB‐48) and liver (apoB‐100), in men with normal fasting triglycerides but at increased risk of developing type 2 diabetes. Design.  Cross‐sectional study. Subjects and settings.  Sixteen healthy men with at least two first‐degree relatives with type 2 diabetes were individually matched with 16 control subjects without known diabetes heredity for: age, body mass index, and fasting triglyceride level. They underwent an 8‐h meal tolerance test (919 kcal, 51 g fat) during which lipoproteins were separated by density gradient ultracentrifugation. They were characterized by euglycaemic hyperinsulinaemic clamp, peak VO2, 7‐day diet registration and computed tomography. Results.  The relatives were, as expected, more insulin resistant than the controls and had increased concentration of postprandial VLDL1 particles (49% higher for VLDL1 apoB‐48, P = 0.04 and 21% higher for VLDL1 apoB‐100, P = 0.048). The elevation was related to insulin sensitivity, but not to lifestyle and body composition. Moreover, the concentration of postprandial triglycerides in VLDL1 fraction was inversely related to low‐density lipoprotein (LDL) size in both relatives (rs = −0.60, P = 0.03) and controls (rs = −0.72, P = 0.004). There were no differences in the concentration of triglycerides or apoB‐48 and apoB‐100 particles in the other fractions (plasma, chylomicron or VLDL2). Conclusion.  Increased postprandial concentration of TRLs in the VLDL1 fraction seems to be present at an early stage in the development of diabetes and probably contributes to the excess risk of future coronary events in insulin‐resistant men.</description><subject>Adult</subject><subject>Anthropometry</subject><subject>Apolipoprotein B-100</subject><subject>Apolipoprotein B-48</subject><subject>Apolipoproteins B - blood</subject><subject>apoproteins</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Cholesterol</subject><subject>Cholesterol, VLDL - blood</subject><subject>Cross-Sectional Studies</subject><subject>Diabetes Mellitus</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>General aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Glucose Tolerance Test</subject><subject>Humans</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>Life Style</subject><subject>Male</subject><subject>MEDICAL AND HEALTH SCIENCES</subject><subject>Medical sciences</subject><subject>MEDICIN OCH HÄLSOVETENSKAP</subject><subject>Middle Aged</subject><subject>Postprandial Period - physiology</subject><subject>post‐prandial</subject><subject>Triglycerides - blood</subject><subject>triglyceride‐rich lipoproteins</subject><subject>Type 2/blood/genetics</subject><subject>VLDL/blood</subject><issn>0954-6820</issn><issn>1365-2796</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqNkc9u1DAQhyMEotvCKyALCU7dZfw32QsSlAJFi3oBrpaTnex6lcSp7WibEzwCz8iT4LBLK3HiZHv8zc8efVlGKCwoCPVqt6BcyTnLl2rBAPgCKCvo4vZBNru7eJjNYCnFXBUMTrLTEHYAlIOCx9kJFblQUslZ9v3S-GYkponoTbSuC8R2JG6R9C7E3ptubU1Dvq3erSgxvXv768dPCkBS_e9RFKTFaErX2NBO3S12ZG_jloToXbchW_S4tnEktfMkjj0SRlJqiRHDk-xRbZqAT4_rWfb1_eWXi4_z1fWHq4s3q3klKdC5LHJRUJAVMLpm0uRYcilqVqIpacFLBUqovEJl8jQhN1xxCVLWiq4R2ZLxs-z8kBv22A-l7r1tjR-1M1Zvhl6n0mbQAbUErlTCXx7w3rubAUPUrQ0VNo3p0A1BF0ApE0wm8Pk_4M4NvkujaLpMlGBLSFBxgCrvQvBY3z1PQU9C9U5P3vTkTU9C9R-h-ja1PjvmD2WL6_vGo8EEvDgCJlSmqZOxyoZ7TkrGIBeJe33g9rbB8b8_oD9dX32etvw3foG8Kw</recordid><startdate>200402</startdate><enddate>200402</enddate><creator>Johanson, E. H.</creator><creator>Jansson, P.‐A.</creator><creator>Gustafson, B.</creator><creator>Lönn, L.</creator><creator>Smith, U.</creator><creator>Taskinen, M.‐R.</creator><creator>Axelsen, M.</creator><general>Blackwell Science Ltd</general><general>Blackwell Science</general><general>Blackwell Publishing Ltd</general><scope>IQODW</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>7QL</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>200402</creationdate><title>Early alterations in the postprandial VLDL1 apoB‐100 and apoB‐48 metabolism in men with strong heredity for type 2 diabetes</title><author>Johanson, E. 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Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>General aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Glucose Tolerance Test</topic><topic>Humans</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>Life Style</topic><topic>Male</topic><topic>MEDICAL AND HEALTH SCIENCES</topic><topic>Medical sciences</topic><topic>MEDICIN OCH HÄLSOVETENSKAP</topic><topic>Middle Aged</topic><topic>Postprandial Period - physiology</topic><topic>post‐prandial</topic><topic>Triglycerides - blood</topic><topic>triglyceride‐rich lipoproteins</topic><topic>Type 2/blood/genetics</topic><topic>VLDL/blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Johanson, E. H.</creatorcontrib><creatorcontrib>Jansson, P.‐A.</creatorcontrib><creatorcontrib>Gustafson, B.</creatorcontrib><creatorcontrib>Lönn, L.</creatorcontrib><creatorcontrib>Smith, U.</creatorcontrib><creatorcontrib>Taskinen, M.‐R.</creatorcontrib><creatorcontrib>Axelsen, M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Journal of internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Johanson, E. H.</au><au>Jansson, P.‐A.</au><au>Gustafson, B.</au><au>Lönn, L.</au><au>Smith, U.</au><au>Taskinen, M.‐R.</au><au>Axelsen, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Early alterations in the postprandial VLDL1 apoB‐100 and apoB‐48 metabolism in men with strong heredity for type 2 diabetes</atitle><jtitle>Journal of internal medicine</jtitle><addtitle>J Intern Med</addtitle><date>2004-02</date><risdate>2004</risdate><volume>255</volume><issue>2</issue><spage>273</spage><epage>279</epage><pages>273-279</pages><issn>0954-6820</issn><eissn>1365-2796</eissn><abstract>. Objectives.  To study the postprandial triglyceride‐rich lipoprotein (TRL) metabolism, specifically the concentrations of very low‐density lipoproteins (VLDL); from intestine (apoB‐48) and liver (apoB‐100), in men with normal fasting triglycerides but at increased risk of developing type 2 diabetes. Design.  Cross‐sectional study. Subjects and settings.  Sixteen healthy men with at least two first‐degree relatives with type 2 diabetes were individually matched with 16 control subjects without known diabetes heredity for: age, body mass index, and fasting triglyceride level. They underwent an 8‐h meal tolerance test (919 kcal, 51 g fat) during which lipoproteins were separated by density gradient ultracentrifugation. They were characterized by euglycaemic hyperinsulinaemic clamp, peak VO2, 7‐day diet registration and computed tomography. Results.  The relatives were, as expected, more insulin resistant than the controls and had increased concentration of postprandial VLDL1 particles (49% higher for VLDL1 apoB‐48, P = 0.04 and 21% higher for VLDL1 apoB‐100, P = 0.048). The elevation was related to insulin sensitivity, but not to lifestyle and body composition. Moreover, the concentration of postprandial triglycerides in VLDL1 fraction was inversely related to low‐density lipoprotein (LDL) size in both relatives (rs = −0.60, P = 0.03) and controls (rs = −0.72, P = 0.004). There were no differences in the concentration of triglycerides or apoB‐48 and apoB‐100 particles in the other fractions (plasma, chylomicron or VLDL2). Conclusion.  Increased postprandial concentration of TRLs in the VLDL1 fraction seems to be present at an early stage in the development of diabetes and probably contributes to the excess risk of future coronary events in insulin‐resistant men.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>14746565</pmid><doi>10.1046/j.1365-2796.2003.01281.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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ispartof Journal of internal medicine, 2004-02, Vol.255 (2), p.273-279
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language eng
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source Wiley-Blackwell Read & Publish Collection
subjects Adult
Anthropometry
Apolipoprotein B-100
Apolipoprotein B-48
Apolipoproteins B - blood
apoproteins
Biological and medical sciences
Blood Glucose - metabolism
Cholesterol
Cholesterol, VLDL - blood
Cross-Sectional Studies
Diabetes Mellitus
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
General aspects
Genetic Predisposition to Disease
Glucose Tolerance Test
Humans
Insulin - blood
Insulin Resistance
Life Style
Male
MEDICAL AND HEALTH SCIENCES
Medical sciences
MEDICIN OCH HÄLSOVETENSKAP
Middle Aged
Postprandial Period - physiology
post‐prandial
Triglycerides - blood
triglyceride‐rich lipoproteins
Type 2/blood/genetics
VLDL/blood
title Early alterations in the postprandial VLDL1 apoB‐100 and apoB‐48 metabolism in men with strong heredity for type 2 diabetes
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