Apelin Inhibits Diet-Induced Obesity by Enhancing Lymphatic and Blood Vessel Integrity
Identifieur interne : 002501 ( Pmc/Checkpoint ); précédent : 002500; suivant : 002502Apelin Inhibits Diet-Induced Obesity by Enhancing Lymphatic and Blood Vessel Integrity
Auteurs : Mika Sawane [Japon] ; Kentaro Kajiya [Japon] ; Hiroyasu Kidoya [Japon] ; Masaya Takagi [Japon] ; Fumitaka Muramatsu [Japon] ; Nobuyuki Takakura [Japon]Source :
- Diabetes [ 0012-1797 ] ; 2013.
Abstract
Angiogenesis is tightly associated with the outgrowth of adipose tissue, leading to obesity, which is a risk factor for type 2 diabetes and hypertension, mainly because expanding adipose tissue requires an increased nutrient supply from blood vessels. Therefore, induction of vessel abnormality by adipokines has been well-studied, whereas how altered vascular function promotes obesity is relatively unexplored. Also, surviving Prox1 heterozygous mice have shown abnormal lymphatic patterning and adult-onset obesity, indicating that accumulation of adipocytes could be closely linked with lymphatic function. Here, we propose a new antiobesity strategy based on enhancement of lymphatic and blood vessel integrity with apelin. Apelin knockout (KO) mice fed a high-fat diet (HFD) showed an obese phenotype associated with abnormal lymphatic and blood vessel enlargement. Fatty acids present in the HFD induced hyperpermeability of endothelial cells, causing adipocyte differentiation, whereas apelin promoted vascular stabilization. Moreover, treatment of apelin KO mice with a selective cyclooxygenase-2 inhibitor, celecoxib, that were fed an HFD improved vascular function and also attenuated obesity. Finally, apelin transgenic mice showed decreased subcutaneous adipose tissue attributable to inhibition of HFD-induced hyperpermeability of vessels. These results indicate that apelin inhibits HFD-induced obesity by enhancing vessel integrity. Apelin could serve as a therapeutic target for treating obesity and related diseases.
Url:
DOI: 10.2337/db12-0604
PubMed: 23378608
PubMed Central: 3661640
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Angiogenesis is tightly associated with the outgrowth of adipose tissue, leading to obesity, which is a risk factor for type 2 diabetes and hypertension, mainly because expanding adipose tissue requires an increased nutrient supply from blood vessels. Therefore, induction of vessel abnormality by adipokines has been well-studied, whereas how altered vascular function promotes obesity is relatively unexplored. Also, surviving Prox1 heterozygous mice have shown abnormal lymphatic patterning and adult-onset obesity, indicating that accumulation of adipocytes could be closely linked with lymphatic function. Here, we propose a new antiobesity strategy based on enhancement of lymphatic and blood vessel integrity with apelin. Apelin knockout (KO) mice fed a high-fat diet (HFD) showed an obese phenotype associated with abnormal lymphatic and blood vessel enlargement. Fatty acids present in the HFD induced hyperpermeability of endothelial cells, causing adipocyte differentiation, whereas apelin promoted vascular stabilization. Moreover, treatment of apelin KO mice with a selective cyclooxygenase-2 inhibitor, celecoxib, that were fed an HFD improved vascular function and also attenuated obesity. Finally, apelin transgenic mice showed decreased subcutaneous adipose tissue attributable to inhibition of HFD-induced hyperpermeability of vessels. These results indicate that apelin inhibits HFD-induced obesity by enhancing vessel integrity. Apelin could serve as a therapeutic target for treating obesity and related diseases.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Diabetes</journal-id>
<journal-id journal-id-type="iso-abbrev">Diabetes</journal-id>
<journal-id journal-id-type="hwp">diabetes</journal-id>
<journal-id journal-id-type="pmc">diabetes</journal-id>
<journal-id journal-id-type="publisher-id">Diabetes</journal-id>
<journal-title-group><journal-title>Diabetes</journal-title>
</journal-title-group>
<issn pub-type="ppub">0012-1797</issn>
<issn pub-type="epub">1939-327X</issn>
<publisher><publisher-name>American Diabetes Association</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23378608</article-id>
<article-id pub-id-type="pmc">3661640</article-id>
<article-id pub-id-type="publisher-id">0604</article-id>
<article-id pub-id-type="doi">10.2337/db12-0604</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject>
<subj-group><subject>Obesity Studies</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Apelin Inhibits Diet-Induced Obesity by Enhancing Lymphatic and Blood Vessel Integrity</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Sawane</surname>
<given-names>Mika</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kajiya</surname>
<given-names>Kentaro</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="corresp" rid="cor1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kidoya</surname>
<given-names>Hiroyasu</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Takagi</surname>
<given-names>Masaya</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Muramatsu</surname>
<given-names>Fumitaka</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Takakura</surname>
<given-names>Nobuyuki</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="corresp" rid="cor1"></xref>
</contrib>
<aff id="aff1"><sup>1</sup>
Department of Signal Transduction, Research Institute of Microbial Diseases, Osaka University, Osaka, Japan</aff>
<aff id="aff2"><sup>2</sup>
Shiseido Innovative Science Research Center, Yokohama, Japan</aff>
</contrib-group>
<author-notes><corresp id="cor1">Corresponding author: Kentaro Kajiya, <email>kentaro.kajiya@to.shiseido.co.jp</email>
, or Nobuyuki Takakura, <email>ntakaku@biken.osaka-u.ac.jp</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>6</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>20</day>
<month>5</month>
<year>2013</year>
</pub-date>
<volume>62</volume>
<issue>6</issue>
<fpage>1970</fpage>
<lpage>1980</lpage>
<history><date date-type="received"><day>09</day>
<month>5</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>25</day>
<month>1</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>© 2013 by the American Diabetes Association.</copyright-statement>
<copyright-year>2013</copyright-year>
<license license-type="creative-commons"><license-p>Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-nd/3.0/">http://creativecommons.org/licenses/by-nc-nd/3.0/</ext-link>
for details.</license-p>
</license>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="1970.pdf"></self-uri>
<abstract><p>Angiogenesis is tightly associated with the outgrowth of adipose tissue, leading to obesity, which is a risk factor for type 2 diabetes and hypertension, mainly because expanding adipose tissue requires an increased nutrient supply from blood vessels. Therefore, induction of vessel abnormality by adipokines has been well-studied, whereas how altered vascular function promotes obesity is relatively unexplored. Also, surviving Prox1 heterozygous mice have shown abnormal lymphatic patterning and adult-onset obesity, indicating that accumulation of adipocytes could be closely linked with lymphatic function. Here, we propose a new antiobesity strategy based on enhancement of lymphatic and blood vessel integrity with apelin. Apelin knockout (KO) mice fed a high-fat diet (HFD) showed an obese phenotype associated with abnormal lymphatic and blood vessel enlargement. Fatty acids present in the HFD induced hyperpermeability of endothelial cells, causing adipocyte differentiation, whereas apelin promoted vascular stabilization. Moreover, treatment of apelin KO mice with a selective cyclooxygenase-2 inhibitor, celecoxib, that were fed an HFD improved vascular function and also attenuated obesity. Finally, apelin transgenic mice showed decreased subcutaneous adipose tissue attributable to inhibition of HFD-induced hyperpermeability of vessels. These results indicate that apelin inhibits HFD-induced obesity by enhancing vessel integrity. Apelin could serve as a therapeutic target for treating obesity and related diseases.</p>
</abstract>
<counts><page-count count="11"></page-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Japon</li>
</country>
</list>
<tree><country name="Japon"><noRegion><name sortKey="Sawane, Mika" sort="Sawane, Mika" uniqKey="Sawane M" first="Mika" last="Sawane">Mika Sawane</name>
</noRegion>
<name sortKey="Kajiya, Kentaro" sort="Kajiya, Kentaro" uniqKey="Kajiya K" first="Kentaro" last="Kajiya">Kentaro Kajiya</name>
<name sortKey="Kidoya, Hiroyasu" sort="Kidoya, Hiroyasu" uniqKey="Kidoya H" first="Hiroyasu" last="Kidoya">Hiroyasu Kidoya</name>
<name sortKey="Muramatsu, Fumitaka" sort="Muramatsu, Fumitaka" uniqKey="Muramatsu F" first="Fumitaka" last="Muramatsu">Fumitaka Muramatsu</name>
<name sortKey="Sawane, Mika" sort="Sawane, Mika" uniqKey="Sawane M" first="Mika" last="Sawane">Mika Sawane</name>
<name sortKey="Takagi, Masaya" sort="Takagi, Masaya" uniqKey="Takagi M" first="Masaya" last="Takagi">Masaya Takagi</name>
<name sortKey="Takakura, Nobuyuki" sort="Takakura, Nobuyuki" uniqKey="Takakura N" first="Nobuyuki" last="Takakura">Nobuyuki Takakura</name>
</country>
</tree>
</affiliations>
</record>
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