Adiponectin acts in the brain to decrease body weight
Adiponectin (ADP) is an adipocyte hormone involved in glucose and lipid metabolism. We detected a rise in ADP in cerebrospinal fluid after intravenous (i.v.) injection, consistent with brain transport. In contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weigh...
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description | Adiponectin (ADP) is an adipocyte hormone involved in glucose and lipid metabolism. We detected a rise in ADP in cerebrospinal fluid after intravenous (i.v.) injection, consistent with brain transport. In contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weight mainly by stimulating energy expenditure. Full-length ADP, mutant ADP with Cys39 replaced with serine, and globular ADP were effective, whereas the collagenous tail fragment was not.
Lep
ob/ob
mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased thermogenesis, weight loss and reduction in serum glucose and lipid levels. ADP also potentiated the effect of leptin on thermogenesis and lipid levels. While both hormones increased expression of hypothalamic corticotropin-releasing hormone (CRH), ADP had no substantial effect on other neuropeptide targets of leptin. In addition, ADP induced distinct Fos immunoreactivity. Agouti (
A
y
/
a
) mice did not respond to ADP or leptin, indicating the melanocortin pathway may be a common target. These results show that ADP has unique central effects on energy homeostasis. |
doi_str_mv | 10.1038/nm1029 |
format | Article |
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Lep
ob/ob
mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased thermogenesis, weight loss and reduction in serum glucose and lipid levels. ADP also potentiated the effect of leptin on thermogenesis and lipid levels. While both hormones increased expression of hypothalamic corticotropin-releasing hormone (CRH), ADP had no substantial effect on other neuropeptide targets of leptin. In addition, ADP induced distinct Fos immunoreactivity. Agouti (
A
y
/
a
) mice did not respond to ADP or leptin, indicating the melanocortin pathway may be a common target. These results show that ADP has unique central effects on energy homeostasis.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/nm1029</identifier><identifier>PMID: 15077108</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Adiponectin ; Agouti Signaling Protein ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Body weight ; Body Weight - drug effects ; Body Weight - physiology ; Brain - physiology ; Cancer Research ; Drug Synergism ; Energy Metabolism - drug effects ; Hormones ; Infectious Diseases ; Injection ; Injections, Intraventricular ; Intercellular Signaling Peptides and Proteins - genetics ; Leptin - administration & dosage ; Metabolic Diseases ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mice, Obese ; Molecular Medicine ; Neurosciences ; Proteins - administration & dosage ; Proteins - physiology ; Recombinant Proteins - administration & dosage</subject><ispartof>Nature medicine, 2004-05, Vol.10 (5), p.524-529</ispartof><rights>Springer Nature America, Inc. 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c607t-cecbbdcb5de4168f835dc8684295d5d9b29d2752d913d84a9b17d6ab19f195c43</citedby><cites>FETCH-LOGICAL-c607t-cecbbdcb5de4168f835dc8684295d5d9b29d2752d913d84a9b17d6ab19f195c43</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/nm1029$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nm1029$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15077108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qi, Yong</creatorcontrib><creatorcontrib>Takahashi, Nobuhiko</creatorcontrib><creatorcontrib>Hileman, Stanley M</creatorcontrib><creatorcontrib>Patel, Hiralben R</creatorcontrib><creatorcontrib>Berg, Anders H</creatorcontrib><creatorcontrib>Pajvani, Utpal B</creatorcontrib><creatorcontrib>Scherer, Philipp E</creatorcontrib><creatorcontrib>Ahima, Rexford S</creatorcontrib><title>Adiponectin acts in the brain to decrease body weight</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>Adiponectin (ADP) is an adipocyte hormone involved in glucose and lipid metabolism. We detected a rise in ADP in cerebrospinal fluid after intravenous (i.v.) injection, consistent with brain transport. In contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weight mainly by stimulating energy expenditure. Full-length ADP, mutant ADP with Cys39 replaced with serine, and globular ADP were effective, whereas the collagenous tail fragment was not.
Lep
ob/ob
mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased thermogenesis, weight loss and reduction in serum glucose and lipid levels. ADP also potentiated the effect of leptin on thermogenesis and lipid levels. While both hormones increased expression of hypothalamic corticotropin-releasing hormone (CRH), ADP had no substantial effect on other neuropeptide targets of leptin. In addition, ADP induced distinct Fos immunoreactivity. Agouti (
A
y
/
a
) mice did not respond to ADP or leptin, indicating the melanocortin pathway may be a common target. These results show that ADP has unique central effects on energy homeostasis.</description><subject>Adiponectin</subject><subject>Agouti Signaling Protein</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body weight</subject><subject>Body Weight - drug effects</subject><subject>Body Weight - physiology</subject><subject>Brain - physiology</subject><subject>Cancer Research</subject><subject>Drug Synergism</subject><subject>Energy Metabolism - drug effects</subject><subject>Hormones</subject><subject>Infectious Diseases</subject><subject>Injection</subject><subject>Injections, Intraventricular</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Leptin - administration & dosage</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Mutant Strains</subject><subject>Mice, Obese</subject><subject>Molecular 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to decrease body weight</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>10</volume><issue>5</issue><spage>524</spage><epage>529</epage><pages>524-529</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>Adiponectin (ADP) is an adipocyte hormone involved in glucose and lipid metabolism. We detected a rise in ADP in cerebrospinal fluid after intravenous (i.v.) injection, consistent with brain transport. In contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weight mainly by stimulating energy expenditure. Full-length ADP, mutant ADP with Cys39 replaced with serine, and globular ADP were effective, whereas the collagenous tail fragment was not.
Lep
ob/ob
mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased thermogenesis, weight loss and reduction in serum glucose and lipid levels. ADP also potentiated the effect of leptin on thermogenesis and lipid levels. While both hormones increased expression of hypothalamic corticotropin-releasing hormone (CRH), ADP had no substantial effect on other neuropeptide targets of leptin. In addition, ADP induced distinct Fos immunoreactivity. Agouti (
A
y
/
a
) mice did not respond to ADP or leptin, indicating the melanocortin pathway may be a common target. These results show that ADP has unique central effects on energy homeostasis.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15077108</pmid><doi>10.1038/nm1029</doi><tpages>6</tpages></addata></record> |
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subjects | Adiponectin Agouti Signaling Protein Animals Biomedical and Life Sciences Biomedicine Body weight Body Weight - drug effects Body Weight - physiology Brain - physiology Cancer Research Drug Synergism Energy Metabolism - drug effects Hormones Infectious Diseases Injection Injections, Intraventricular Intercellular Signaling Peptides and Proteins - genetics Leptin - administration & dosage Metabolic Diseases Mice Mice, Inbred C57BL Mice, Mutant Strains Mice, Obese Molecular Medicine Neurosciences Proteins - administration & dosage Proteins - physiology Recombinant Proteins - administration & dosage |
title | Adiponectin acts in the brain to decrease body weight |
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