Insulin resistance is not a major determinant of low-density lipoprotein particle size
The relationship between low-density lipoprotein (LDL) peak particle diameter and insulin sensitivity, very—low-density lipoprotein (VLDL) + intermediate-density lipoprotein (LDL) triglyceride, cholesterol, and apoprotein B, postprandial lipemia, and LDL + high-density lipoprotein (HDL) triglyceride...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 1997-11, Vol.46 (11), p.1275-1280 |
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creator | Slyper, Arnold H. Zvereva, Svetlana Schechtman, Gordon Hoffmann, Raymond G. Mueller, Robert A. Walker, John A. |
description | The relationship between low-density lipoprotein (LDL) peak particle diameter and insulin sensitivity, very—low-density lipoprotein (VLDL) + intermediate-density lipoprotein (LDL) triglyceride, cholesterol, and apoprotein B, postprandial lipemia, and LDL + high-density lipoprotein (HDL) triglyceride was assessed. The subjects were 101 healthy males aged 15 to 45 years. Sixty-one subjects (60.4%) were offspring of a parent with coronary artery disease before age 60, and 40 subjects (39.6%) had no parental history of coronary artery disease. LDL peak particle diameter was measured following polyacrylamide gradient gel electrophoresis. An insulin sensitivity index (S
i) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. A fat tolerance test was performed with a test meal containing 70 g/m
2 fat, with triglyceride concentrations measured hourly for 12 hours. LDL peak particle diameter was significantly correlated with body mass index (BMI) (
r = −.282,
P < .01), waist to hip ratio (
r = −.291,
P < .01), fasting triglyceride (logarithmically [log] transformed) (
r = −.556,
P < .001), area under the postprandial triglyceride (log transformed) (
r = −.562,
P < .001), VLDL + IDLL triglyceride (log transformed) (
r = −.321,
P < .001), LDL + HDLL triglyceride (log transformed) (
r = .583,
P < .001), and HDL cholesterol (
r = .347,
P < .001), but there was no significant correlation with S
i. Using stepwise regression analysis, LDL + HDL triglyceride showed the strongest relationship to LDL peak particle diameter, accounting for 34% of the variation in size. S
I was not an independent predictor of LDL particle size. In conclusion, insulin sensitivity appears to have little influence on LDL particle size. The importance of LDL + HDL triglyceride should be ocnsidered a preliminary finding warranting varification in this and other populations. |
doi_str_mv | 10.1016/S0026-0495(97)90230-4 |
format | Article |
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i) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. A fat tolerance test was performed with a test meal containing 70 g/m
2 fat, with triglyceride concentrations measured hourly for 12 hours. LDL peak particle diameter was significantly correlated with body mass index (BMI) (
r = −.282,
P < .01), waist to hip ratio (
r = −.291,
P < .01), fasting triglyceride (logarithmically [log] transformed) (
r = −.556,
P < .001), area under the postprandial triglyceride (log transformed) (
r = −.562,
P < .001), VLDL + IDLL triglyceride (log transformed) (
r = −.321,
P < .001), LDL + HDLL triglyceride (log transformed) (
r = .583,
P < .001), and HDL cholesterol (
r = .347,
P < .001), but there was no significant correlation with S
i. Using stepwise regression analysis, LDL + HDL triglyceride showed the strongest relationship to LDL peak particle diameter, accounting for 34% of the variation in size. S
I was not an independent predictor of LDL particle size. In conclusion, insulin sensitivity appears to have little influence on LDL particle size. The importance of LDL + HDL triglyceride should be ocnsidered a preliminary finding warranting varification in this and other populations.]]></description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/S0026-0495(97)90230-4</identifier><identifier>PMID: 9361685</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Biological and medical sciences ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fasting - blood ; Humans ; Insulin Resistance - physiology ; Lipoproteins, LDL - chemistry ; Male ; Medical sciences ; Middle Aged ; Particle Size ; Regression Analysis ; Triglycerides - blood</subject><ispartof>Metabolism, clinical and experimental, 1997-11, Vol.46 (11), p.1275-1280</ispartof><rights>1997</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-1c982b2f526904dbe5868eaf518ab82d13a1354de09ea7cf4cd6b347569d8fe53</citedby><cites>FETCH-LOGICAL-c389t-1c982b2f526904dbe5868eaf518ab82d13a1354de09ea7cf4cd6b347569d8fe53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0026-0495(97)90230-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2057493$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9361685$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Slyper, Arnold H.</creatorcontrib><creatorcontrib>Zvereva, Svetlana</creatorcontrib><creatorcontrib>Schechtman, Gordon</creatorcontrib><creatorcontrib>Hoffmann, Raymond G.</creatorcontrib><creatorcontrib>Mueller, Robert A.</creatorcontrib><creatorcontrib>Walker, John A.</creatorcontrib><title>Insulin resistance is not a major determinant of low-density lipoprotein particle size</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description><![CDATA[The relationship between low-density lipoprotein (LDL) peak particle diameter and insulin sensitivity, very—low-density lipoprotein (VLDL) + intermediate-density lipoprotein (LDL) triglyceride, cholesterol, and apoprotein B, postprandial lipemia, and LDL + high-density lipoprotein (HDL) triglyceride was assessed. The subjects were 101 healthy males aged 15 to 45 years. Sixty-one subjects (60.4%) were offspring of a parent with coronary artery disease before age 60, and 40 subjects (39.6%) had no parental history of coronary artery disease. LDL peak particle diameter was measured following polyacrylamide gradient gel electrophoresis. An insulin sensitivity index (S
i) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. A fat tolerance test was performed with a test meal containing 70 g/m
2 fat, with triglyceride concentrations measured hourly for 12 hours. LDL peak particle diameter was significantly correlated with body mass index (BMI) (
r = −.282,
P < .01), waist to hip ratio (
r = −.291,
P < .01), fasting triglyceride (logarithmically [log] transformed) (
r = −.556,
P < .001), area under the postprandial triglyceride (log transformed) (
r = −.562,
P < .001), VLDL + IDLL triglyceride (log transformed) (
r = −.321,
P < .001), LDL + HDLL triglyceride (log transformed) (
r = .583,
P < .001), and HDL cholesterol (
r = .347,
P < .001), but there was no significant correlation with S
i. Using stepwise regression analysis, LDL + HDL triglyceride showed the strongest relationship to LDL peak particle diameter, accounting for 34% of the variation in size. S
I was not an independent predictor of LDL particle size. In conclusion, insulin sensitivity appears to have little influence on LDL particle size. The importance of LDL + HDL triglyceride should be ocnsidered a preliminary finding warranting varification in this and other populations.]]></description><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</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>Fasting - blood</subject><subject>Humans</subject><subject>Insulin Resistance - physiology</subject><subject>Lipoproteins, LDL - chemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Particle Size</subject><subject>Regression Analysis</subject><subject>Triglycerides - blood</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1rFTEUhoMo9bb6EwpZiNTF2HxMMslKpFQtFFxU3YZMcgZSZibXnNxK_fWmvZe7dXUW73POeXkIOefsI2dcX94xJnTHeqsu7PDBMiFZ178gG66k6Ixm7CXZHJHX5BTxnjE2DEafkBMrNddGbcivmxV3c1ppAUxY_RqAJqRrrtTTxd_nQiNUKEta_Vppnuic_3QRVkz1kc5pm7clV2gHtr7UFGagmP7CG_Jq8jPC28M8Iz-_XP-4-tbdfv96c_X5tgvS2NrxYI0YxaSEtqyPIyijDfhJceNHIyKXnkvVR2AW_BCmPkQ9yn5Q2kYzgZJn5P3-bmvxewdY3ZIwwDz7FfIO3WCltVKJBqo9GEpGLDC5bUmLL4-OM_fk0z37dE-ynB3cs0_Xt73zw4PduEA8bh0EtvzdIfcY_DyVZjDhERNMDb2VDfu0x6DJeEhQHIYETXZMBUJ1Maf_FPkHDMWSvA</recordid><startdate>19971101</startdate><enddate>19971101</enddate><creator>Slyper, Arnold H.</creator><creator>Zvereva, Svetlana</creator><creator>Schechtman, Gordon</creator><creator>Hoffmann, Raymond G.</creator><creator>Mueller, Robert A.</creator><creator>Walker, John A.</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>19971101</creationdate><title>Insulin resistance is not a major determinant of low-density lipoprotein particle size</title><author>Slyper, Arnold H. ; Zvereva, Svetlana ; Schechtman, Gordon ; Hoffmann, Raymond G. ; Mueller, Robert A. ; Walker, John A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-1c982b2f526904dbe5868eaf518ab82d13a1354de09ea7cf4cd6b347569d8fe53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fasting - blood</topic><topic>Humans</topic><topic>Insulin Resistance - physiology</topic><topic>Lipoproteins, LDL - chemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Particle Size</topic><topic>Regression Analysis</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Slyper, Arnold H.</creatorcontrib><creatorcontrib>Zvereva, Svetlana</creatorcontrib><creatorcontrib>Schechtman, Gordon</creatorcontrib><creatorcontrib>Hoffmann, Raymond G.</creatorcontrib><creatorcontrib>Mueller, Robert A.</creatorcontrib><creatorcontrib>Walker, John A.</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>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Slyper, Arnold H.</au><au>Zvereva, Svetlana</au><au>Schechtman, Gordon</au><au>Hoffmann, Raymond G.</au><au>Mueller, Robert A.</au><au>Walker, John A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin resistance is not a major determinant of low-density lipoprotein particle size</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>1997-11-01</date><risdate>1997</risdate><volume>46</volume><issue>11</issue><spage>1275</spage><epage>1280</epage><pages>1275-1280</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract><![CDATA[The relationship between low-density lipoprotein (LDL) peak particle diameter and insulin sensitivity, very—low-density lipoprotein (VLDL) + intermediate-density lipoprotein (LDL) triglyceride, cholesterol, and apoprotein B, postprandial lipemia, and LDL + high-density lipoprotein (HDL) triglyceride was assessed. The subjects were 101 healthy males aged 15 to 45 years. Sixty-one subjects (60.4%) were offspring of a parent with coronary artery disease before age 60, and 40 subjects (39.6%) had no parental history of coronary artery disease. LDL peak particle diameter was measured following polyacrylamide gradient gel electrophoresis. An insulin sensitivity index (S
i) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. A fat tolerance test was performed with a test meal containing 70 g/m
2 fat, with triglyceride concentrations measured hourly for 12 hours. LDL peak particle diameter was significantly correlated with body mass index (BMI) (
r = −.282,
P < .01), waist to hip ratio (
r = −.291,
P < .01), fasting triglyceride (logarithmically [log] transformed) (
r = −.556,
P < .001), area under the postprandial triglyceride (log transformed) (
r = −.562,
P < .001), VLDL + IDLL triglyceride (log transformed) (
r = −.321,
P < .001), LDL + HDLL triglyceride (log transformed) (
r = .583,
P < .001), and HDL cholesterol (
r = .347,
P < .001), but there was no significant correlation with S
i. Using stepwise regression analysis, LDL + HDL triglyceride showed the strongest relationship to LDL peak particle diameter, accounting for 34% of the variation in size. S
I was not an independent predictor of LDL particle size. In conclusion, insulin sensitivity appears to have little influence on LDL particle size. The importance of LDL + HDL triglyceride should be ocnsidered a preliminary finding warranting varification in this and other populations.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>9361685</pmid><doi>10.1016/S0026-0495(97)90230-4</doi><tpages>6</tpages></addata></record> |
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source | MEDLINE; Access via ScienceDirect (Elsevier) |
subjects | Adolescent Adult Biological and medical sciences Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fasting - blood Humans Insulin Resistance - physiology Lipoproteins, LDL - chemistry Male Medical sciences Middle Aged Particle Size Regression Analysis Triglycerides - blood |
title | Insulin resistance is not a major determinant of low-density lipoprotein particle size |
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