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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Veröffentlicht in:International Journal of Obesity 2008-06, Vol.32 (6), p.936-942
Hauptverfasser: Asensio, C.S, Arsenijevic, D, Lehr, L, Giacobino, J.P, Muzzin, P, Rohner-Jeanrenaud, F
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container_issue 6
container_start_page 936
container_title International Journal of Obesity
container_volume 32
creator Asensio, C.S
Arsenijevic, D
Lehr, L
Giacobino, J.P
Muzzin, P
Rohner-Jeanrenaud, F
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 &amp; 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&amp;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. 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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. 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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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