Effects of leptin on energy metabolism in β-less mice
Objective: To investigate the impact of β-adrenoceptor deficiency on the metabolic effects of leptin. Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and β1/β2/β3-adrenoceptor knockout (β-less) mice and its effects on food intake, energy expenditure, car...
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description | Objective: To investigate the impact of β-adrenoceptor deficiency on the metabolic effects of leptin. Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and β1/β2/β3-adrenoceptor knockout (β-less) mice and its effects on food intake, energy expenditure, carbohydrate and lipid utilization as well as on the levels of expression of the brown adipose tissue (BAT), thermogenic marker uncoupling protein-1 (UCP1) and type II deiodinase (D2) mRNAs were compared. Results: Leptin treatment decreased food intake by 23% in both the WT and the β-less mice. In pair-fed animals being used as controls, leptin treatment was found to increase energy expenditure in WT, but not in β-less mice. No difference was observed in carbohydrate or fat utilization between leptin-treated WT and β-less mice. Leptin increased UCP1 and D2 mRNA levels in WT mouse BAT 1.7- and 3-fold, respectively, but had no effect on the expression of these genes in β-less mouse BAT. Conclusion: The stimulatory effects of leptin on oxygen consumption, BAT UCP1 and D2 expression require functional β-adrenoceptors, but its inhibitory effect on food intake and its stimulatory effect on fat utilization is independent of the β-adrenoceptor signalling. |
doi_str_mv | 10.1038/ijo.2008.13 |
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Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and β1/β2/β3-adrenoceptor knockout (β-less) mice and its effects on food intake, energy expenditure, carbohydrate and lipid utilization as well as on the levels of expression of the brown adipose tissue (BAT), thermogenic marker uncoupling protein-1 (UCP1) and type II deiodinase (D2) mRNAs were compared. Results: Leptin treatment decreased food intake by 23% in both the WT and the β-less mice. In pair-fed animals being used as controls, leptin treatment was found to increase energy expenditure in WT, but not in β-less mice. No difference was observed in carbohydrate or fat utilization between leptin-treated WT and β-less mice. Leptin increased UCP1 and D2 mRNA levels in WT mouse BAT 1.7- and 3-fold, respectively, but had no effect on the expression of these genes in β-less mouse BAT. Conclusion: The stimulatory effects of leptin on oxygen consumption, BAT UCP1 and D2 expression require functional β-adrenoceptors, but its inhibitory effect on food intake and its stimulatory effect on fat utilization is independent of the β-adrenoceptor signalling.</description><identifier>ISSN: 0307-0565</identifier><identifier>EISSN: 1476-5497</identifier><identifier>DOI: 10.1038/ijo.2008.13</identifier><identifier>PMID: 18283283</identifier><identifier>CODEN: IJOBDP</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adipose Tissue, Brown - drug effects ; Adipose Tissue, Brown - metabolism ; adrenergic receptors ; Analysis ; animal models ; animal proteins ; Animals ; Bioenergetics ; Biological and medical sciences ; Brown adipose tissue ; Calorimetry, Indirect - methods ; carbohydrate metabolism ; Dosage and administration ; energy expenditure ; Energy Intake - drug effects ; Energy metabolism ; Energy Metabolism - drug effects ; Epidemiology ; Feeding Methods ; food intake ; Genetically modified mice ; Health aspects ; Health Promotion and Disease Prevention ; Internal Medicine ; Iodide Peroxidase - metabolism ; Iodothyronine Deiodinase Type II ; Ion Channels - metabolism ; knockout mutants ; Leptin ; Leptin - pharmacology ; lipid metabolism ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; messenger RNA ; Metabolic Diseases ; Mice ; Mice, Knockout ; Mitochondrial Proteins - metabolism ; Obesity ; original-article ; Polymerase Chain Reaction ; protein synthesis ; Public Health ; Receptors, Adrenergic, beta - deficiency ; Receptors, Adrenergic, beta - physiology ; RNA, Messenger - metabolism ; Uncoupling Protein 1</subject><ispartof>International Journal of Obesity, 2008-06, Vol.32 (6), p.936-942</ispartof><rights>Springer Nature Limited 2008</rights><rights>2008 INIST-CNRS</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-d00862fb5629530f14abac8003121613c69e1314e5db13ffc51cb6826b86b6093</citedby><cites>FETCH-LOGICAL-c531t-d00862fb5629530f14abac8003121613c69e1314e5db13ffc51cb6826b86b6093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ijo.2008.13$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ijo.2008.13$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27915,27916,41479,42548,51310</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20418925$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18283283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asensio, C.S</creatorcontrib><creatorcontrib>Arsenijevic, D</creatorcontrib><creatorcontrib>Lehr, L</creatorcontrib><creatorcontrib>Giacobino, J.P</creatorcontrib><creatorcontrib>Muzzin, P</creatorcontrib><creatorcontrib>Rohner-Jeanrenaud, F</creatorcontrib><title>Effects of leptin on energy metabolism in β-less mice</title><title>International Journal of Obesity</title><addtitle>Int J Obes</addtitle><addtitle>Int J Obes (Lond)</addtitle><description>Objective: To investigate the impact of β-adrenoceptor deficiency on the metabolic effects of leptin. Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and β1/β2/β3-adrenoceptor knockout (β-less) mice and its effects on food intake, energy expenditure, carbohydrate and lipid utilization as well as on the levels of expression of the brown adipose tissue (BAT), thermogenic marker uncoupling protein-1 (UCP1) and type II deiodinase (D2) mRNAs were compared. Results: Leptin treatment decreased food intake by 23% in both the WT and the β-less mice. In pair-fed animals being used as controls, leptin treatment was found to increase energy expenditure in WT, but not in β-less mice. No difference was observed in carbohydrate or fat utilization between leptin-treated WT and β-less mice. Leptin increased UCP1 and D2 mRNA levels in WT mouse BAT 1.7- and 3-fold, respectively, but had no effect on the expression of these genes in β-less mouse BAT. Conclusion: The stimulatory effects of leptin on oxygen consumption, BAT UCP1 and D2 expression require functional β-adrenoceptors, but its inhibitory effect on food intake and its stimulatory effect on fat utilization is independent of the β-adrenoceptor signalling.</description><subject>Adipose Tissue, Brown - drug effects</subject><subject>Adipose Tissue, Brown - metabolism</subject><subject>adrenergic receptors</subject><subject>Analysis</subject><subject>animal models</subject><subject>animal proteins</subject><subject>Animals</subject><subject>Bioenergetics</subject><subject>Biological and medical sciences</subject><subject>Brown adipose tissue</subject><subject>Calorimetry, Indirect - methods</subject><subject>carbohydrate metabolism</subject><subject>Dosage and administration</subject><subject>energy expenditure</subject><subject>Energy Intake - drug effects</subject><subject>Energy metabolism</subject><subject>Energy Metabolism - drug effects</subject><subject>Epidemiology</subject><subject>Feeding Methods</subject><subject>food intake</subject><subject>Genetically modified mice</subject><subject>Health aspects</subject><subject>Health Promotion and Disease Prevention</subject><subject>Internal Medicine</subject><subject>Iodide Peroxidase - metabolism</subject><subject>Iodothyronine Deiodinase Type II</subject><subject>Ion Channels - metabolism</subject><subject>knockout mutants</subject><subject>Leptin</subject><subject>Leptin - pharmacology</subject><subject>lipid metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>messenger RNA</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Obesity</subject><subject>original-article</subject><subject>Polymerase Chain Reaction</subject><subject>protein synthesis</subject><subject>Public Health</subject><subject>Receptors, Adrenergic, beta - deficiency</subject><subject>Receptors, Adrenergic, beta - physiology</subject><subject>RNA, Messenger - metabolism</subject><subject>Uncoupling Protein 1</subject><issn>0307-0565</issn><issn>1476-5497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c9rFDEUB_BBFLtWT951oLQXnfW9ZJLNHEupP6DgQXsOmezLdpaZZE1mDv23_EP8m5p1ltqCIgkEkk_y8vgWxWuEJQJXH7ptWDIAtUT-pFhgvZKVqJvV02IBHFYVCCmOihcpbQFACGDPiyNUTPE8F4W8dI7smMrgyp52Y-fL4EvyFDe35UCjaUPfpaHM-79-Vj2lVA6dpZfFM2f6RK8O63Fx_fHy-8Xn6urrpy8X51eVFRzHap2_JZlrhWSN4OCwNq2xCoAjQ4ncyoaQY01i3SJ3zgq0rVRMtkq2Ehp-XJzN7-5i-DFRGvXQJUt9bzyFKWnZMORCwX8hA7USnIkMT2a4MT3pzrswRmP3WJ9jAyiQcZnV8i8qjzXl9oMn1-X9RxfOHly4IdOPNyn009gFnx7DdzO0MaQUyeld7AYTbzWC3uepc556n6dGnvWbQ1tTO9D6jz0EmMHpAZhkTe-i8bZL945Bjar53fb72aV85DcU9TZM0efs_lH37cy9GadI9-9lsycPhTNBm03MRa-_MUAO0GAuqPgdyGjF9A</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Asensio, C.S</creator><creator>Arsenijevic, D</creator><creator>Lehr, L</creator><creator>Giacobino, J.P</creator><creator>Muzzin, P</creator><creator>Rohner-Jeanrenaud, F</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>FBQ</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>7QG</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20080601</creationdate><title>Effects of leptin on energy metabolism in β-less mice</title><author>Asensio, C.S ; Arsenijevic, D ; Lehr, L ; Giacobino, J.P ; Muzzin, P ; Rohner-Jeanrenaud, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-d00862fb5629530f14abac8003121613c69e1314e5db13ffc51cb6826b86b6093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adipose Tissue, Brown - drug effects</topic><topic>Adipose Tissue, Brown - metabolism</topic><topic>adrenergic receptors</topic><topic>Analysis</topic><topic>animal models</topic><topic>animal proteins</topic><topic>Animals</topic><topic>Bioenergetics</topic><topic>Biological and medical sciences</topic><topic>Brown adipose tissue</topic><topic>Calorimetry, Indirect - methods</topic><topic>carbohydrate metabolism</topic><topic>Dosage and administration</topic><topic>energy expenditure</topic><topic>Energy Intake - drug effects</topic><topic>Energy metabolism</topic><topic>Energy Metabolism - drug effects</topic><topic>Epidemiology</topic><topic>Feeding Methods</topic><topic>food intake</topic><topic>Genetically modified mice</topic><topic>Health aspects</topic><topic>Health Promotion and Disease Prevention</topic><topic>Internal Medicine</topic><topic>Iodide Peroxidase - metabolism</topic><topic>Iodothyronine Deiodinase Type II</topic><topic>Ion Channels - metabolism</topic><topic>knockout mutants</topic><topic>Leptin</topic><topic>Leptin - pharmacology</topic><topic>lipid metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>messenger RNA</topic><topic>Metabolic Diseases</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Obesity</topic><topic>original-article</topic><topic>Polymerase Chain Reaction</topic><topic>protein synthesis</topic><topic>Public Health</topic><topic>Receptors, Adrenergic, beta - deficiency</topic><topic>Receptors, Adrenergic, beta - physiology</topic><topic>RNA, Messenger - metabolism</topic><topic>Uncoupling Protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asensio, C.S</creatorcontrib><creatorcontrib>Arsenijevic, D</creatorcontrib><creatorcontrib>Lehr, L</creatorcontrib><creatorcontrib>Giacobino, J.P</creatorcontrib><creatorcontrib>Muzzin, P</creatorcontrib><creatorcontrib>Rohner-Jeanrenaud, F</creatorcontrib><collection>AGRIS</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>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International Journal of Obesity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asensio, C.S</au><au>Arsenijevic, D</au><au>Lehr, L</au><au>Giacobino, J.P</au><au>Muzzin, P</au><au>Rohner-Jeanrenaud, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of leptin on energy metabolism in β-less mice</atitle><jtitle>International Journal of Obesity</jtitle><stitle>Int J Obes</stitle><addtitle>Int J Obes (Lond)</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>32</volume><issue>6</issue><spage>936</spage><epage>942</epage><pages>936-942</pages><issn>0307-0565</issn><eissn>1476-5497</eissn><coden>IJOBDP</coden><abstract>Objective: To investigate the impact of β-adrenoceptor deficiency on the metabolic effects of leptin. Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and β1/β2/β3-adrenoceptor knockout (β-less) mice and its effects on food intake, energy expenditure, carbohydrate and lipid utilization as well as on the levels of expression of the brown adipose tissue (BAT), thermogenic marker uncoupling protein-1 (UCP1) and type II deiodinase (D2) mRNAs were compared. Results: Leptin treatment decreased food intake by 23% in both the WT and the β-less mice. In pair-fed animals being used as controls, leptin treatment was found to increase energy expenditure in WT, but not in β-less mice. No difference was observed in carbohydrate or fat utilization between leptin-treated WT and β-less mice. Leptin increased UCP1 and D2 mRNA levels in WT mouse BAT 1.7- and 3-fold, respectively, but had no effect on the expression of these genes in β-less mouse BAT. Conclusion: The stimulatory effects of leptin on oxygen consumption, BAT UCP1 and D2 expression require functional β-adrenoceptors, but its inhibitory effect on food intake and its stimulatory effect on fat utilization is independent of the β-adrenoceptor signalling.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18283283</pmid><doi>10.1038/ijo.2008.13</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - metabolism adrenergic receptors Analysis animal models animal proteins Animals Bioenergetics Biological and medical sciences Brown adipose tissue Calorimetry, Indirect - methods carbohydrate metabolism Dosage and administration energy expenditure Energy Intake - drug effects Energy metabolism Energy Metabolism - drug effects Epidemiology Feeding Methods food intake Genetically modified mice Health aspects Health Promotion and Disease Prevention Internal Medicine Iodide Peroxidase - metabolism Iodothyronine Deiodinase Type II Ion Channels - metabolism knockout mutants Leptin Leptin - pharmacology lipid metabolism Male Medical sciences Medicine Medicine & Public Health messenger RNA Metabolic Diseases Mice Mice, Knockout Mitochondrial Proteins - metabolism Obesity original-article Polymerase Chain Reaction protein synthesis Public Health Receptors, Adrenergic, beta - deficiency Receptors, Adrenergic, beta - physiology RNA, Messenger - metabolism Uncoupling Protein 1 |
title | Effects of leptin on energy metabolism in β-less mice |
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