Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity
Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity. L Plum , R Kluge , K Giesen , J Altmüller , J R Ortlepp and H G Joost Institute of Pharmacology and Toxicology, Medical Faculty of th...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2000-09, Vol.49 (9), p.1590-1596 |
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| container_title | Diabetes (New York, N.Y.) |
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| creator | Plum, L Kluge, R Giesen, K Altmüller, J Ortlepp, J R Joost, H G |
| description | Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on
chromosome 4 and its relation with obesity.
L Plum ,
R Kluge ,
K Giesen ,
J Altmüller ,
J R Ortlepp and
H G Joost
Institute of Pharmacology and Toxicology, Medical Faculty of the Technical University Aachen, Germany.
Abstract
A backcross model of New Zealand obese mice (NZO) with the lean, atherosclerosis-resistant SJL strain was established to locate
genes responsible for obesity, insulin resistance, and type 2 diabetes-like hyperglycemia. In male NZO x F1 backcross mice,
a major susceptibility locus for the development of hyperglycemia and hypoinsulinemia (Nidd/SJL) was identified on chromosome
4 between the markers D4Mit278 and D4Mit232, 10-28 cM distal of the previously described Nidd1 locus. The diabetogenic allele
has presumably been contributed by the SJL genome, and it appeared to be responsible for approximately 60% of the total prevalence
of hyperglycemia. The presence of Nidd/SJL did not alter body weight or weight gain by week 12. Thereafter, it was associated
with reduced weight gain or weight loss, presumably as a consequence of decompensated hyperglycemia. In all male backcross
mice, the prevalence of hyperglycemia at week 22 increased with the body weight at week 12, suggesting that the development
of hyperglycemia was dependent on the degree of obesity. In the absence of Nidd/SJL, mice weighing |
| doi_str_mv | 10.2337/diabetes.49.9.1590 |
| format | Article |
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chromosome 4 and its relation with obesity.
L Plum ,
R Kluge ,
K Giesen ,
J Altmüller ,
J R Ortlepp and
H G Joost
Institute of Pharmacology and Toxicology, Medical Faculty of the Technical University Aachen, Germany.
Abstract
A backcross model of New Zealand obese mice (NZO) with the lean, atherosclerosis-resistant SJL strain was established to locate
genes responsible for obesity, insulin resistance, and type 2 diabetes-like hyperglycemia. In male NZO x F1 backcross mice,
a major susceptibility locus for the development of hyperglycemia and hypoinsulinemia (Nidd/SJL) was identified on chromosome
4 between the markers D4Mit278 and D4Mit232, 10-28 cM distal of the previously described Nidd1 locus. The diabetogenic allele
has presumably been contributed by the SJL genome, and it appeared to be responsible for approximately 60% of the total prevalence
of hyperglycemia. The presence of Nidd/SJL did not alter body weight or weight gain by week 12. Thereafter, it was associated
with reduced weight gain or weight loss, presumably as a consequence of decompensated hyperglycemia. In all male backcross
mice, the prevalence of hyperglycemia at week 22 increased with the body weight at week 12, suggesting that the development
of hyperglycemia was dependent on the degree of obesity. In the absence of Nidd/SJL, mice weighing <50 g at week 12 did not
develop hyperglycemia by week 22. In contrast, in animals carrying the diabetogenic allele, the prevalence of hyperglycemia
was 20 and 64% when the 12-week weight was <45 and 45-50 g, respectively. These data are consistent with the conclusion that
Nidd/SJL represents a diabetes gene that lowers the obesity threshold for the development of hyperglycemia and hypoinsulinemia.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/diabetes.49.9.1590</identifier><identifier>PMID: 10969845</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Aging ; Animals ; Associated diseases and complications ; Biological and medical sciences ; Blood Glucose - metabolism ; Body Mass Index ; Body Weight ; Cholesterol - blood ; Chromosome Mapping ; Crosses, Genetic ; Diabetes ; Diabetes Mellitus - blood ; Diabetes Mellitus - genetics ; Diabetes Mellitus - physiopathology ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Female ; Genetic Predisposition to Disease - genetics ; Genomes ; Hyperglycemia ; Hyperglycemia - blood ; Hyperglycemia - genetics ; Hyperglycemia - physiopathology ; Insulin - blood ; Insulin resistance ; Laboratory animals ; Male ; Medical sciences ; Metabolism ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Obesity ; Obesity - blood ; Obesity - genetics ; Obesity - physiopathology ; Triglycerides - blood ; Weight control</subject><ispartof>Diabetes (New York, N.Y.), 2000-09, Vol.49 (9), p.1590-1596</ispartof><rights>2001 INIST-CNRS</rights><rights>Copyright American Diabetes Association Sep 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-8cf4b5012d462c182acd0de32e2ff3d0c2e0a69ef697000403a31e7671b2f7ba3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=788467$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10969845$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Plum, L</creatorcontrib><creatorcontrib>Kluge, R</creatorcontrib><creatorcontrib>Giesen, K</creatorcontrib><creatorcontrib>Altmüller, J</creatorcontrib><creatorcontrib>Ortlepp, J R</creatorcontrib><creatorcontrib>Joost, H G</creatorcontrib><title>Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on
chromosome 4 and its relation with obesity.
L Plum ,
R Kluge ,
K Giesen ,
J Altmüller ,
J R Ortlepp and
H G Joost
Institute of Pharmacology and Toxicology, Medical Faculty of the Technical University Aachen, Germany.
Abstract
A backcross model of New Zealand obese mice (NZO) with the lean, atherosclerosis-resistant SJL strain was established to locate
genes responsible for obesity, insulin resistance, and type 2 diabetes-like hyperglycemia. In male NZO x F1 backcross mice,
a major susceptibility locus for the development of hyperglycemia and hypoinsulinemia (Nidd/SJL) was identified on chromosome
4 between the markers D4Mit278 and D4Mit232, 10-28 cM distal of the previously described Nidd1 locus. The diabetogenic allele
has presumably been contributed by the SJL genome, and it appeared to be responsible for approximately 60% of the total prevalence
of hyperglycemia. The presence of Nidd/SJL did not alter body weight or weight gain by week 12. Thereafter, it was associated
with reduced weight gain or weight loss, presumably as a consequence of decompensated hyperglycemia. In all male backcross
mice, the prevalence of hyperglycemia at week 22 increased with the body weight at week 12, suggesting that the development
of hyperglycemia was dependent on the degree of obesity. In the absence of Nidd/SJL, mice weighing <50 g at week 12 did not
develop hyperglycemia by week 22. In contrast, in animals carrying the diabetogenic allele, the prevalence of hyperglycemia
was 20 and 64% when the 12-week weight was <45 and 45-50 g, respectively. These data are consistent with the conclusion that
Nidd/SJL represents a diabetes gene that lowers the obesity threshold for the development of hyperglycemia and hypoinsulinemia.</description><subject>Aging</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body Mass Index</subject><subject>Body Weight</subject><subject>Cholesterol - blood</subject><subject>Chromosome Mapping</subject><subject>Crosses, Genetic</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - blood</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes Mellitus - physiopathology</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genomes</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - blood</subject><subject>Hyperglycemia - genetics</subject><subject>Hyperglycemia - physiopathology</subject><subject>Insulin - blood</subject><subject>Insulin resistance</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Mutant Strains</subject><subject>Obesity</subject><subject>Obesity - blood</subject><subject>Obesity - genetics</subject><subject>Obesity - physiopathology</subject><subject>Triglycerides - blood</subject><subject>Weight control</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1u1DAUhS0EokPhBVggCyQ2KIP_EsfsUMVfNaILioTYWI5z07h14sFOVA3vw3viaaYFIeSFJd_vnHt9LkJPKVkzzuXr1pkGJkhrodZqTUtF7qEVVVwVnMlv99GKEMoKKpU8Qo9SuiSEVPk8REeUqErVolyhX-e7LWCGb70K764A9_kxXvidhcEZ7EZscGPslY0hJTyEFjwOHf78_QybscVfTjd4cBbeYNubaOwE0f00kwvjnjI4zcnCdnKN827aYR_snHAu2j6GIaQwABY3Rm5KOIJfpNdu6nFoIGXNY_SgMz7Bk8N9jL6-f3d-8rHYnH34dPJ2U1jBxVTUthNNmT_diopZWjNjW9ICZ8C6jrfEMiCmUtBVSuYwBOGGU5CVpA3rZGP4MXq5-G5j-DFDmvTg8uzemxHCnLRkjJWyLjP4_B_wMsxxzLNpRitRVzneDLEFusktQqe30Q0m7jQler9BfZu6Fkorvd9gFj07OM_NAO1fkmVlGXhxAEyyxnfRjNalO07Wtahkpl4tVO8u-msX4U-v_zT9DXyatvs</recordid><startdate>20000901</startdate><enddate>20000901</enddate><creator>Plum, L</creator><creator>Kluge, R</creator><creator>Giesen, K</creator><creator>Altmüller, J</creator><creator>Ortlepp, J R</creator><creator>Joost, H G</creator><general>American Diabetes Association</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20000901</creationdate><title>Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity</title><author>Plum, L ; Kluge, R ; Giesen, K ; Altmüller, J ; Ortlepp, J R ; Joost, H G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-8cf4b5012d462c182acd0de32e2ff3d0c2e0a69ef697000403a31e7671b2f7ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Body Mass Index</topic><topic>Body Weight</topic><topic>Cholesterol - blood</topic><topic>Chromosome Mapping</topic><topic>Crosses, Genetic</topic><topic>Diabetes</topic><topic>Diabetes Mellitus - blood</topic><topic>Diabetes Mellitus - genetics</topic><topic>Diabetes Mellitus - physiopathology</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genomes</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - blood</topic><topic>Hyperglycemia - genetics</topic><topic>Hyperglycemia - physiopathology</topic><topic>Insulin - blood</topic><topic>Insulin resistance</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Mutant Strains</topic><topic>Obesity</topic><topic>Obesity - blood</topic><topic>Obesity - genetics</topic><topic>Obesity - physiopathology</topic><topic>Triglycerides - blood</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Plum, L</creatorcontrib><creatorcontrib>Kluge, R</creatorcontrib><creatorcontrib>Giesen, K</creatorcontrib><creatorcontrib>Altmüller, J</creatorcontrib><creatorcontrib>Ortlepp, J R</creatorcontrib><creatorcontrib>Joost, H G</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plum, L</au><au>Kluge, R</au><au>Giesen, K</au><au>Altmüller, J</au><au>Ortlepp, J R</au><au>Joost, H G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2000-09-01</date><risdate>2000</risdate><volume>49</volume><issue>9</issue><spage>1590</spage><epage>1596</epage><pages>1590-1596</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on
chromosome 4 and its relation with obesity.
L Plum ,
R Kluge ,
K Giesen ,
J Altmüller ,
J R Ortlepp and
H G Joost
Institute of Pharmacology and Toxicology, Medical Faculty of the Technical University Aachen, Germany.
Abstract
A backcross model of New Zealand obese mice (NZO) with the lean, atherosclerosis-resistant SJL strain was established to locate
genes responsible for obesity, insulin resistance, and type 2 diabetes-like hyperglycemia. In male NZO x F1 backcross mice,
a major susceptibility locus for the development of hyperglycemia and hypoinsulinemia (Nidd/SJL) was identified on chromosome
4 between the markers D4Mit278 and D4Mit232, 10-28 cM distal of the previously described Nidd1 locus. The diabetogenic allele
has presumably been contributed by the SJL genome, and it appeared to be responsible for approximately 60% of the total prevalence
of hyperglycemia. The presence of Nidd/SJL did not alter body weight or weight gain by week 12. Thereafter, it was associated
with reduced weight gain or weight loss, presumably as a consequence of decompensated hyperglycemia. In all male backcross
mice, the prevalence of hyperglycemia at week 22 increased with the body weight at week 12, suggesting that the development
of hyperglycemia was dependent on the degree of obesity. In the absence of Nidd/SJL, mice weighing <50 g at week 12 did not
develop hyperglycemia by week 22. In contrast, in animals carrying the diabetogenic allele, the prevalence of hyperglycemia
was 20 and 64% when the 12-week weight was <45 and 45-50 g, respectively. These data are consistent with the conclusion that
Nidd/SJL represents a diabetes gene that lowers the obesity threshold for the development of hyperglycemia and hypoinsulinemia.</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>10969845</pmid><doi>10.2337/diabetes.49.9.1590</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetes (New York, N.Y.), 2000-09, Vol.49 (9), p.1590-1596 |
| issn | 0012-1797 1939-327X |
| language | eng |
| recordid | cdi_proquest_journals_216486698 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Aging Animals Associated diseases and complications Biological and medical sciences Blood Glucose - metabolism Body Mass Index Body Weight Cholesterol - blood Chromosome Mapping Crosses, Genetic Diabetes Diabetes Mellitus - blood Diabetes Mellitus - genetics Diabetes Mellitus - physiopathology Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - physiopathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Female Genetic Predisposition to Disease - genetics Genomes Hyperglycemia Hyperglycemia - blood Hyperglycemia - genetics Hyperglycemia - physiopathology Insulin - blood Insulin resistance Laboratory animals Male Medical sciences Metabolism Mice Mice, Inbred Strains Mice, Mutant Strains Obesity Obesity - blood Obesity - genetics Obesity - physiopathology Triglycerides - blood Weight control |
| title | Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice: characterization of a susceptibility locus on chromosome 4 and its relation with obesity |
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