Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency
Background We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL −/−, homozygotes), and have contrasted these with heterozygotes (LPL +/−) and normal c...
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| Veröffentlicht in: | European journal of clinical investigation 1999-01, Vol.29 (1), p.17-26 |
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| creator | GINZINGER, D. G CLEE, S. M INNIS, S JONES, B FRUCHART, J.-C HAYDEN, M. R DALLONGEVILLE, J LEWIS, M. E. S HENDERSON, H. E BAUJE, E ROGERS, Q. R JENSEN, D. R ECKEL, R. H DYER, R |
| description | Background
We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL −/−, homozygotes), and have contrasted these with heterozygotes (LPL +/−) and normal cats (LPL +/+).
Materials and methods
Density gradient ultracentrifugation with subsequent lipid analysis, agarose and polyacrylamide gel electrophoresis was used to examine detailed liproprotein differences between the genotypes. Oral fat loading studies and breast milk fatty acid analysis were also performed to further characterize the phenotypic expression of LPL deficiency in this model system.
Results
Several lipid abnormalities associated with homozygosity for LPL deficiency were evident. Triglyceride‐rich lipoprotein‐triglycerides (TRL‐TG) and cholesterol (TRL‐C) were higher (TRL‐TG 2.09 ± 1.14 vs. 0.15 ± 0.04 mmol L−1, P |
| doi_str_mv | 10.1046/j.1365-2362.1999.00435.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69646966</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>39413838</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4585-960272e0bc2373875c06e889d5fdbaf8fdf37a2b3ce7e34370fa98a3c1437e773</originalsourceid><addsrcrecordid>eNqNkF1r2zAUhsXYWNNsf2GYMXpn90iy9QG7GaFrA6G76NbBboQiHzFljp1ZDk3-_eQ5dB9XBQkdoec9kh5CMgoFhVJcbgrKRZUzLlhBtdYFQMmr4vCMzB4PnpMZAC1zpiU7I-cxbgBAUc5ekjMKoJlW5YwsV2EX6sy2ddaEXbfruwFDm_a2OcYQs85nzg4xewjD93-IVNuIWY0-uICtO74iL7xtIr4-rXPy5ePV58VNvvp0vVx8WOWurFSVawFMMoS1Y1xyJSsHApXSdeXrtfXK155Ly9bcoURecgneamW5o6lGKfmcXEx900t-7jEOZhuiw6axLXb7aIQWZZoigW__Azfdvk8fiyY5A8lZkjYnaoJc38XYoze7PmxtfzQUzOjabMyo1IxKx5w2v12bQ4q-OfXfr7dY_xWc5Cbg3Qmw0dnG97Z1If7hhExjfOf7CXsIDR6ffL-5WixTkeL5FA9xwMNj3PY_jJBcVubr7bW5FyW7p6tv5o7_Aj-fqDo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>199073204</pqid></control><display><type>article</type><title>Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>GINZINGER, D. G ; CLEE, S. M ; INNIS, S ; JONES, B ; FRUCHART, J.-C ; HAYDEN, M. R ; DALLONGEVILLE, J ; LEWIS, M. E. S ; HENDERSON, H. E ; BAUJE, E ; ROGERS, Q. R ; JENSEN, D. R ; ECKEL, R. H ; DYER, R</creator><creatorcontrib>GINZINGER, D. G ; CLEE, S. M ; INNIS, S ; JONES, B ; FRUCHART, J.-C ; HAYDEN, M. R ; DALLONGEVILLE, J ; LEWIS, M. E. S ; HENDERSON, H. E ; BAUJE, E ; ROGERS, Q. R ; JENSEN, D. R ; ECKEL, R. H ; DYER, R</creatorcontrib><description>Background
We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL −/−, homozygotes), and have contrasted these with heterozygotes (LPL +/−) and normal cats (LPL +/+).
Materials and methods
Density gradient ultracentrifugation with subsequent lipid analysis, agarose and polyacrylamide gel electrophoresis was used to examine detailed liproprotein differences between the genotypes. Oral fat loading studies and breast milk fatty acid analysis were also performed to further characterize the phenotypic expression of LPL deficiency in this model system.
Results
Several lipid abnormalities associated with homozygosity for LPL deficiency were evident. Triglyceride‐rich lipoprotein‐triglycerides (TRL‐TG) and cholesterol (TRL‐C) were higher (TRL‐TG 2.09 ± 1.14 vs. 0.15 ± 0.04 mmol L−1, P < 0.001; TRL‐C 0.42 ± 0.30 vs. 0.11 ± 0.16 mmol L−1, P < 0.05) in male −/− than in male +/+ cats, as was HDL‐cholesterol (HDL‐C, 1.75 ± 0.24 vs. 1.41 ± 0.14 mmol L−1, P < 0.05). LDL‐C levels were lower in homozygous cats than in control cats, similar to what is seen in human LPL deficiency. Oral fat loading studies revealed that homozygous cats have a marked reduced ability to clear plasma TGs in terms of peak time (7 h vs. 3 h), peak height (9.36 vs. 1.1 mmol L−1), area under the TG clearance curve (AUC, 280.3 vs. 2.2 h mmol L−1) and time to return to baseline. Fasting lipid and lipoprotein levels were not significantly different between heterozygous and normal cats. However, oral fat loading in heterozygotes revealed an intermediate phenotype (peak of 2.35 mmol L−1 at 5 h, AUC 13.1 h mmol L−1), highlighting the impaired TG clearance in these animals.
Conclusion
Thus, LPL deficiency in the cat results in a lipid and lipoprotein phenotype that predominantly parallels human LPL deficiency, further validating the use of these animals in studies on the pathobiology of LPL.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1046/j.1365-2362.1999.00435.x</identifier><identifier>PMID: 10092984</identifier><language>eng</language><publisher>Oxford BSL: Blackwell Science Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blood Chemical Analysis ; Cats ; Cats - genetics ; Cats - metabolism ; Cholesterol - blood ; Dietary Fats - metabolism ; Disorders of blood lipids. Hyperlipoproteinemia ; Fatty Acids - analysis ; Female ; Heterozygote ; Homozygote ; Lactation ; Lipids - analysis ; lipoprotein lipase ; Lipoprotein Lipase - deficiency ; Lipoprotein Lipase - genetics ; lipoproteins ; Lipoproteins - blood ; Male ; Medical sciences ; Metabolic diseases ; Milk - chemistry ; milk fatty acids ; Mutation ; oral fat load ; particle composition ; Particle Size ; Postprandial Period ; Triglycerides - blood</subject><ispartof>European journal of clinical investigation, 1999-01, Vol.29 (1), p.17-26</ispartof><rights>Blackwell Science Ltd, Oxford</rights><rights>1999 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Jan 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4585-960272e0bc2373875c06e889d5fdbaf8fdf37a2b3ce7e34370fa98a3c1437e773</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2362.1999.00435.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2362.1999.00435.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,4024,27923,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1671676$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10092984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GINZINGER, D. G</creatorcontrib><creatorcontrib>CLEE, S. M</creatorcontrib><creatorcontrib>INNIS, S</creatorcontrib><creatorcontrib>JONES, B</creatorcontrib><creatorcontrib>FRUCHART, J.-C</creatorcontrib><creatorcontrib>HAYDEN, M. R</creatorcontrib><creatorcontrib>DALLONGEVILLE, J</creatorcontrib><creatorcontrib>LEWIS, M. E. S</creatorcontrib><creatorcontrib>HENDERSON, H. E</creatorcontrib><creatorcontrib>BAUJE, E</creatorcontrib><creatorcontrib>ROGERS, Q. R</creatorcontrib><creatorcontrib>JENSEN, D. R</creatorcontrib><creatorcontrib>ECKEL, R. H</creatorcontrib><creatorcontrib>DYER, R</creatorcontrib><title>Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency</title><title>European journal of clinical investigation</title><addtitle>European Journal of Clinical Investigation</addtitle><description>Background
We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL −/−, homozygotes), and have contrasted these with heterozygotes (LPL +/−) and normal cats (LPL +/+).
Materials and methods
Density gradient ultracentrifugation with subsequent lipid analysis, agarose and polyacrylamide gel electrophoresis was used to examine detailed liproprotein differences between the genotypes. Oral fat loading studies and breast milk fatty acid analysis were also performed to further characterize the phenotypic expression of LPL deficiency in this model system.
Results
Several lipid abnormalities associated with homozygosity for LPL deficiency were evident. Triglyceride‐rich lipoprotein‐triglycerides (TRL‐TG) and cholesterol (TRL‐C) were higher (TRL‐TG 2.09 ± 1.14 vs. 0.15 ± 0.04 mmol L−1, P < 0.001; TRL‐C 0.42 ± 0.30 vs. 0.11 ± 0.16 mmol L−1, P < 0.05) in male −/− than in male +/+ cats, as was HDL‐cholesterol (HDL‐C, 1.75 ± 0.24 vs. 1.41 ± 0.14 mmol L−1, P < 0.05). LDL‐C levels were lower in homozygous cats than in control cats, similar to what is seen in human LPL deficiency. Oral fat loading studies revealed that homozygous cats have a marked reduced ability to clear plasma TGs in terms of peak time (7 h vs. 3 h), peak height (9.36 vs. 1.1 mmol L−1), area under the TG clearance curve (AUC, 280.3 vs. 2.2 h mmol L−1) and time to return to baseline. Fasting lipid and lipoprotein levels were not significantly different between heterozygous and normal cats. However, oral fat loading in heterozygotes revealed an intermediate phenotype (peak of 2.35 mmol L−1 at 5 h, AUC 13.1 h mmol L−1), highlighting the impaired TG clearance in these animals.
Conclusion
Thus, LPL deficiency in the cat results in a lipid and lipoprotein phenotype that predominantly parallels human LPL deficiency, further validating the use of these animals in studies on the pathobiology of LPL.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Chemical Analysis</subject><subject>Cats</subject><subject>Cats - genetics</subject><subject>Cats - metabolism</subject><subject>Cholesterol - blood</subject><subject>Dietary Fats - metabolism</subject><subject>Disorders of blood lipids. Hyperlipoproteinemia</subject><subject>Fatty Acids - analysis</subject><subject>Female</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Lactation</subject><subject>Lipids - analysis</subject><subject>lipoprotein lipase</subject><subject>Lipoprotein Lipase - deficiency</subject><subject>Lipoprotein Lipase - genetics</subject><subject>lipoproteins</subject><subject>Lipoproteins - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Milk - chemistry</subject><subject>milk fatty acids</subject><subject>Mutation</subject><subject>oral fat load</subject><subject>particle composition</subject><subject>Particle Size</subject><subject>Postprandial Period</subject><subject>Triglycerides - blood</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkF1r2zAUhsXYWNNsf2GYMXpn90iy9QG7GaFrA6G76NbBboQiHzFljp1ZDk3-_eQ5dB9XBQkdoec9kh5CMgoFhVJcbgrKRZUzLlhBtdYFQMmr4vCMzB4PnpMZAC1zpiU7I-cxbgBAUc5ekjMKoJlW5YwsV2EX6sy2ddaEXbfruwFDm_a2OcYQs85nzg4xewjD93-IVNuIWY0-uICtO74iL7xtIr4-rXPy5ePV58VNvvp0vVx8WOWurFSVawFMMoS1Y1xyJSsHApXSdeXrtfXK155Ly9bcoURecgneamW5o6lGKfmcXEx900t-7jEOZhuiw6axLXb7aIQWZZoigW__Azfdvk8fiyY5A8lZkjYnaoJc38XYoze7PmxtfzQUzOjabMyo1IxKx5w2v12bQ4q-OfXfr7dY_xWc5Cbg3Qmw0dnG97Z1If7hhExjfOf7CXsIDR6ffL-5WixTkeL5FA9xwMNj3PY_jJBcVubr7bW5FyW7p6tv5o7_Aj-fqDo</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>GINZINGER, D. G</creator><creator>CLEE, S. M</creator><creator>INNIS, S</creator><creator>JONES, B</creator><creator>FRUCHART, J.-C</creator><creator>HAYDEN, M. R</creator><creator>DALLONGEVILLE, J</creator><creator>LEWIS, M. E. S</creator><creator>HENDERSON, H. E</creator><creator>BAUJE, E</creator><creator>ROGERS, Q. R</creator><creator>JENSEN, D. R</creator><creator>ECKEL, R. H</creator><creator>DYER, R</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><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>7QO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>199901</creationdate><title>Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency</title><author>GINZINGER, D. G ; CLEE, S. M ; INNIS, S ; JONES, B ; FRUCHART, J.-C ; HAYDEN, M. R ; DALLONGEVILLE, J ; LEWIS, M. E. S ; HENDERSON, H. E ; BAUJE, E ; ROGERS, Q. R ; JENSEN, D. R ; ECKEL, R. H ; DYER, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4585-960272e0bc2373875c06e889d5fdbaf8fdf37a2b3ce7e34370fa98a3c1437e773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Chemical Analysis</topic><topic>Cats</topic><topic>Cats - genetics</topic><topic>Cats - metabolism</topic><topic>Cholesterol - blood</topic><topic>Dietary Fats - metabolism</topic><topic>Disorders of blood lipids. Hyperlipoproteinemia</topic><topic>Fatty Acids - analysis</topic><topic>Female</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Lactation</topic><topic>Lipids - analysis</topic><topic>lipoprotein lipase</topic><topic>Lipoprotein Lipase - deficiency</topic><topic>Lipoprotein Lipase - genetics</topic><topic>lipoproteins</topic><topic>Lipoproteins - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Milk - chemistry</topic><topic>milk fatty acids</topic><topic>Mutation</topic><topic>oral fat load</topic><topic>particle composition</topic><topic>Particle Size</topic><topic>Postprandial Period</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GINZINGER, D. G</creatorcontrib><creatorcontrib>CLEE, S. M</creatorcontrib><creatorcontrib>INNIS, S</creatorcontrib><creatorcontrib>JONES, B</creatorcontrib><creatorcontrib>FRUCHART, J.-C</creatorcontrib><creatorcontrib>HAYDEN, M. R</creatorcontrib><creatorcontrib>DALLONGEVILLE, J</creatorcontrib><creatorcontrib>LEWIS, M. E. S</creatorcontrib><creatorcontrib>HENDERSON, H. E</creatorcontrib><creatorcontrib>BAUJE, E</creatorcontrib><creatorcontrib>ROGERS, Q. R</creatorcontrib><creatorcontrib>JENSEN, D. R</creatorcontrib><creatorcontrib>ECKEL, R. H</creatorcontrib><creatorcontrib>DYER, R</creatorcontrib><collection>Istex</collection><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>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GINZINGER, D. G</au><au>CLEE, S. M</au><au>INNIS, S</au><au>JONES, B</au><au>FRUCHART, J.-C</au><au>HAYDEN, M. R</au><au>DALLONGEVILLE, J</au><au>LEWIS, M. E. S</au><au>HENDERSON, H. E</au><au>BAUJE, E</au><au>ROGERS, Q. R</au><au>JENSEN, D. R</au><au>ECKEL, R. H</au><au>DYER, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>European Journal of Clinical Investigation</addtitle><date>1999-01</date><risdate>1999</risdate><volume>29</volume><issue>1</issue><spage>17</spage><epage>26</epage><pages>17-26</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Background
We have previously described a colony of domestic cats with a naturally occurring mutation in the lipoprotein lipase (LPL) gene. We have now further characterized cats homozygous for LPL deficiency (LPL −/−, homozygotes), and have contrasted these with heterozygotes (LPL +/−) and normal cats (LPL +/+).
Materials and methods
Density gradient ultracentrifugation with subsequent lipid analysis, agarose and polyacrylamide gel electrophoresis was used to examine detailed liproprotein differences between the genotypes. Oral fat loading studies and breast milk fatty acid analysis were also performed to further characterize the phenotypic expression of LPL deficiency in this model system.
Results
Several lipid abnormalities associated with homozygosity for LPL deficiency were evident. Triglyceride‐rich lipoprotein‐triglycerides (TRL‐TG) and cholesterol (TRL‐C) were higher (TRL‐TG 2.09 ± 1.14 vs. 0.15 ± 0.04 mmol L−1, P < 0.001; TRL‐C 0.42 ± 0.30 vs. 0.11 ± 0.16 mmol L−1, P < 0.05) in male −/− than in male +/+ cats, as was HDL‐cholesterol (HDL‐C, 1.75 ± 0.24 vs. 1.41 ± 0.14 mmol L−1, P < 0.05). LDL‐C levels were lower in homozygous cats than in control cats, similar to what is seen in human LPL deficiency. Oral fat loading studies revealed that homozygous cats have a marked reduced ability to clear plasma TGs in terms of peak time (7 h vs. 3 h), peak height (9.36 vs. 1.1 mmol L−1), area under the TG clearance curve (AUC, 280.3 vs. 2.2 h mmol L−1) and time to return to baseline. Fasting lipid and lipoprotein levels were not significantly different between heterozygous and normal cats. However, oral fat loading in heterozygotes revealed an intermediate phenotype (peak of 2.35 mmol L−1 at 5 h, AUC 13.1 h mmol L−1), highlighting the impaired TG clearance in these animals.
Conclusion
Thus, LPL deficiency in the cat results in a lipid and lipoprotein phenotype that predominantly parallels human LPL deficiency, further validating the use of these animals in studies on the pathobiology of LPL.</abstract><cop>Oxford BSL</cop><pub>Blackwell Science Ltd</pub><pmid>10092984</pmid><doi>10.1046/j.1365-2362.1999.00435.x</doi><tpages>10</tpages></addata></record> |
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| ispartof | European journal of clinical investigation, 1999-01, Vol.29 (1), p.17-26 |
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| subjects | Animals Biological and medical sciences Blood Chemical Analysis Cats Cats - genetics Cats - metabolism Cholesterol - blood Dietary Fats - metabolism Disorders of blood lipids. Hyperlipoproteinemia Fatty Acids - analysis Female Heterozygote Homozygote Lactation Lipids - analysis lipoprotein lipase Lipoprotein Lipase - deficiency Lipoprotein Lipase - genetics lipoproteins Lipoproteins - blood Male Medical sciences Metabolic diseases Milk - chemistry milk fatty acids Mutation oral fat load particle composition Particle Size Postprandial Period Triglycerides - blood |
| title | Lipid and lipoprotein analysis of cats with lipoprotein lipase deficiency |
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