Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome
Background/Aims: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic...
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| Veröffentlicht in: | Annals of nutrition and metabolism 2010, Vol.56 (2), p.127-142 |
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| creator | Miesel, Anja Müller, Helge Thermann, Margot Heidbreder, Marc Dominiak, Peter Raasch, Walter |
| description | Background/Aims: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. Methods: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. Results: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Conclusion: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS. |
| doi_str_mv | 10.1159/000278748 |
| format | Article |
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We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. Methods: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. Results: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Conclusion: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS.</description><identifier>ISSN: 0250-6807</identifier><identifier>EISSN: 1421-9697</identifier><identifier>DOI: 10.1159/000278748</identifier><identifier>PMID: 20134158</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Abdominal Fat ; animal disease models ; Animal models ; Animals ; appetite ; Biomarkers - blood ; Blood Glucose ; Blood Pressure ; Body Weight ; C-Peptide - blood ; Diet ; Diet - adverse effects ; Diet - methods ; diet-related diseases ; Disease Models, Animal ; eating habits ; Energy Intake ; epidemiological studies ; Heart Rate ; hypercholesterolemia ; Hyperphagia - blood ; Hyperphagia - complications ; Hypertension ; Insulin - blood ; Insulin Resistance ; leptin ; Leptin - blood ; leptin resistance ; Male ; Metabolic disorders ; Metabolic syndrome ; Metabolic Syndrome - blood ; Metabolic Syndrome - etiology ; nutrition-genotype interaction ; Obesity ; Obesity - blood ; Obesity - etiology ; Original Paper ; overeating ; overweight ; Rats ; Rats, Inbred SHR ; Rats, Sprague-Dawley ; risk factors ; Rodents ; Triglycerides - blood</subject><ispartof>Annals of nutrition and metabolism, 2010, Vol.56 (2), p.127-142</ispartof><rights>2010 S. Karger AG</rights><rights>2010 S. Karger AG, Basel</rights><rights>Copyright 2010 S. Karger AG, Basel.</rights><rights>Copyright (c) 2010 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-9863d170672a0746a263d3b10765179d4316d0969cf82ea01b670910c0c34b973</citedby><cites>FETCH-LOGICAL-c444t-9863d170672a0746a263d3b10765179d4316d0969cf82ea01b670910c0c34b973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/48507074$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/48507074$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2423,4010,27900,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20134158$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miesel, Anja</creatorcontrib><creatorcontrib>Müller, Helge</creatorcontrib><creatorcontrib>Thermann, Margot</creatorcontrib><creatorcontrib>Heidbreder, Marc</creatorcontrib><creatorcontrib>Dominiak, Peter</creatorcontrib><creatorcontrib>Raasch, Walter</creatorcontrib><title>Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome</title><title>Annals of nutrition and metabolism</title><addtitle>Ann Nutr Metab</addtitle><description>Background/Aims: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. Methods: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. Results: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Conclusion: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS.</description><subject>Abdominal Fat</subject><subject>animal disease models</subject><subject>Animal models</subject><subject>Animals</subject><subject>appetite</subject><subject>Biomarkers - blood</subject><subject>Blood Glucose</subject><subject>Blood Pressure</subject><subject>Body Weight</subject><subject>C-Peptide - blood</subject><subject>Diet</subject><subject>Diet - adverse effects</subject><subject>Diet - methods</subject><subject>diet-related diseases</subject><subject>Disease Models, Animal</subject><subject>eating habits</subject><subject>Energy Intake</subject><subject>epidemiological studies</subject><subject>Heart Rate</subject><subject>hypercholesterolemia</subject><subject>Hyperphagia - blood</subject><subject>Hyperphagia - complications</subject><subject>Hypertension</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>leptin</subject><subject>Leptin - blood</subject><subject>leptin resistance</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - etiology</subject><subject>nutrition-genotype interaction</subject><subject>Obesity</subject><subject>Obesity - blood</subject><subject>Obesity - etiology</subject><subject>Original Paper</subject><subject>overeating</subject><subject>overweight</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Sprague-Dawley</subject><subject>risk factors</subject><subject>Rodents</subject><subject>Triglycerides - blood</subject><issn>0250-6807</issn><issn>1421-9697</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpFkEtr3DAUhUVpaaZpF933IbLrwu2VrIfdXQhtJpAw0GnWRraup556pKkkB_zvq-A8QHAR57vncg4h7xl8ZUzW3wCA60qL6gVZMcFZUatavyQr4BIKVYE-IW9i3AMwXgn5mpxwYKVgsloRv7nD0CPawe2KK2enDi3dtBiHNNPB0e3Ru2Qc-imOM13PRwwJXRzukP4yKX6n5y6_4WBGeuMtjtT3NP1Bup4OxtEbTKb149DR7exs8Ad8S171Zoz47mGektufP35frIvrzeXVxfl10QkhUlFXqrRMg9LcgBbK8PwvWwZaSaZrK0qmLOSYXV9xNMBapaFm0EFXirbW5Sk5W3yPwf-bMKZm76fg8slGCclLIZnM0JcF6oKPMWDfHEOOEuaGQXPfbPPUbGY_PRhO7QHtE_lYZQY-LMBfE3YYnoHH_Y-LvI_JP6uikqBzwqx_XvTe-MbswhCb2-29ObCKScmh_A8VuI0h</recordid><startdate>2010</startdate><enddate>2010</enddate><creator>Miesel, Anja</creator><creator>Müller, Helge</creator><creator>Thermann, Margot</creator><creator>Heidbreder, Marc</creator><creator>Dominiak, Peter</creator><creator>Raasch, Walter</creator><general>S. Karger AG</general><scope>FBQ</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>7QP</scope><scope>7RV</scope><scope>7X2</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>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</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>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>2010</creationdate><title>Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome</title><author>Miesel, Anja ; Müller, Helge ; Thermann, Margot ; Heidbreder, Marc ; Dominiak, Peter ; Raasch, Walter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-9863d170672a0746a263d3b10765179d4316d0969cf82ea01b670910c0c34b973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Abdominal Fat</topic><topic>animal disease models</topic><topic>Animal models</topic><topic>Animals</topic><topic>appetite</topic><topic>Biomarkers - blood</topic><topic>Blood Glucose</topic><topic>Blood Pressure</topic><topic>Body Weight</topic><topic>C-Peptide - blood</topic><topic>Diet</topic><topic>Diet - adverse effects</topic><topic>Diet - methods</topic><topic>diet-related diseases</topic><topic>Disease Models, Animal</topic><topic>eating habits</topic><topic>Energy Intake</topic><topic>epidemiological studies</topic><topic>Heart Rate</topic><topic>hypercholesterolemia</topic><topic>Hyperphagia - blood</topic><topic>Hyperphagia - complications</topic><topic>Hypertension</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>leptin</topic><topic>Leptin - blood</topic><topic>leptin resistance</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - blood</topic><topic>Metabolic Syndrome - etiology</topic><topic>nutrition-genotype interaction</topic><topic>Obesity</topic><topic>Obesity - blood</topic><topic>Obesity - etiology</topic><topic>Original Paper</topic><topic>overeating</topic><topic>overweight</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Sprague-Dawley</topic><topic>risk factors</topic><topic>Rodents</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miesel, Anja</creatorcontrib><creatorcontrib>Müller, Helge</creatorcontrib><creatorcontrib>Thermann, Margot</creatorcontrib><creatorcontrib>Heidbreder, Marc</creatorcontrib><creatorcontrib>Dominiak, Peter</creatorcontrib><creatorcontrib>Raasch, Walter</creatorcontrib><collection>AGRIS</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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Agricultural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</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>Agricultural Science Database</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>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 Basic</collection><jtitle>Annals of nutrition and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miesel, Anja</au><au>Müller, Helge</au><au>Thermann, Margot</au><au>Heidbreder, Marc</au><au>Dominiak, Peter</au><au>Raasch, Walter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome</atitle><jtitle>Annals of nutrition and metabolism</jtitle><addtitle>Ann Nutr Metab</addtitle><date>2010</date><risdate>2010</risdate><volume>56</volume><issue>2</issue><spage>127</spage><epage>142</epage><pages>127-142</pages><issn>0250-6807</issn><eissn>1421-9697</eissn><abstract>Background/Aims: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. Methods: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. Results: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Conclusion: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>20134158</pmid><doi>10.1159/000278748</doi><tpages>16</tpages></addata></record> |
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| subjects | Abdominal Fat animal disease models Animal models Animals appetite Biomarkers - blood Blood Glucose Blood Pressure Body Weight C-Peptide - blood Diet Diet - adverse effects Diet - methods diet-related diseases Disease Models, Animal eating habits Energy Intake epidemiological studies Heart Rate hypercholesterolemia Hyperphagia - blood Hyperphagia - complications Hypertension Insulin - blood Insulin Resistance leptin Leptin - blood leptin resistance Male Metabolic disorders Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - etiology nutrition-genotype interaction Obesity Obesity - blood Obesity - etiology Original Paper overeating overweight Rats Rats, Inbred SHR Rats, Sprague-Dawley risk factors Rodents Triglycerides - blood |
| title | Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome |
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