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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">REGULATION OF OBESITY AND INSULIN RESISTANCE BY NITRIC OXIDE</title><author><name sortKey="Sansbury, Brian E" sort="Sansbury, Brian E" uniqKey="Sansbury B" first="Brian E." last="Sansbury">Brian E. Sansbury</name><affiliation><nlm:aff id="A1">Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation></author><author><name sortKey="Hill, Bradford G" sort="Hill, Bradford G" uniqKey="Hill B" first="Bradford G." last="Hill">Bradford G. Hill</name><affiliation><nlm:aff id="A1">Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24878261</idno><idno type="pmc">4112002</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112002</idno><idno type="RBID">PMC:4112002</idno><idno type="doi">10.1016/j.freeradbiomed.2014.05.016</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000347</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000347</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">REGULATION OF OBESITY AND INSULIN RESISTANCE BY NITRIC OXIDE</title><author><name sortKey="Sansbury, Brian E" sort="Sansbury, Brian E" uniqKey="Sansbury B" first="Brian E." last="Sansbury">Brian E. Sansbury</name><affiliation><nlm:aff id="A1">Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation></author><author><name sortKey="Hill, Bradford G" sort="Hill, Bradford G" uniqKey="Hill B" first="Bradford G." last="Hill">Bradford G. Hill</name><affiliation><nlm:aff id="A1">Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY</nlm:aff></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="ISSN">0891-5849</idno><idno type="eISSN">1873-4596</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Obesity is a risk factor for developing type 2 diabetes and cardiovascular disease and has quickly become a world-wide pandemic with few tangible and safe treatment options. While it is generally accepted that the primary cause of obesity is energy imbalance, i.e., the calories consumed are greater than are utilized, understanding how caloric balance is regulated has proven a challenge. Many “distal” causes of obesity, such as the structural environment, occupation, and social influences, are exceedingly difficult to change or manipulate. Hence, molecular processes and pathways more proximal to the origins of obesity—those that directly regulate energy metabolism or caloric intake—appear to be more feasible targets for therapy. In particular, nitric oxide (NO) is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance. This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8709159</journal-id><journal-id journal-id-type="pubmed-jr-id">3902</journal-id><journal-id journal-id-type="nlm-ta">Free Radic Biol Med</journal-id><journal-id journal-id-type="iso-abbrev">Free Radic. Biol. Med.</journal-id><journal-title-group><journal-title>Free radical biology & medicine</journal-title></journal-title-group><issn pub-type="ppub">0891-5849</issn><issn pub-type="epub">1873-4596</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24878261</article-id><article-id pub-id-type="pmc">4112002</article-id><article-id pub-id-type="doi">10.1016/j.freeradbiomed.2014.05.016</article-id><article-id pub-id-type="manuscript">NIHMS600940</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>REGULATION OF OBESITY AND INSULIN RESISTANCE BY NITRIC OXIDE</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Sansbury</surname><given-names>Brian E.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Hill</surname><given-names>Bradford G.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref></contrib></contrib-group><aff id="A1"><label>1</label>Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY</aff><aff id="A2"><label>2</label>Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY</aff><aff id="A3"><label>3</label>Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY</aff><author-notes><corresp id="CR1"><bold>Corresponding Author:</bold> Bradford G. Hill, Ph.D., Department of Medicine, Institute of Molecular Cardiology, Diabetes and Obesity Center, University of Louisville, 580 S. Preston St., Rm 404A, Louisville, KY, 40202; Tel: (502) 852-1015, Fax: (502) 852-3663, <email>bradford.hill@louisville.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>11</day><month>6</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>28</day><month>5</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>8</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>8</month><year>2015</year></pub-date><volume>0</volume><fpage>383</fpage><lpage>399</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.freeradbiomed.2014.05.016</pmc-comment>
<permissions><copyright-statement>© 2014 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year></permissions><abstract><p id="P1">Obesity is a risk factor for developing type 2 diabetes and cardiovascular disease and has quickly become a world-wide pandemic with few tangible and safe treatment options. While it is generally accepted that the primary cause of obesity is energy imbalance, i.e., the calories consumed are greater than are utilized, understanding how caloric balance is regulated has proven a challenge. Many “distal” causes of obesity, such as the structural environment, occupation, and social influences, are exceedingly difficult to change or manipulate. Hence, molecular processes and pathways more proximal to the origins of obesity—those that directly regulate energy metabolism or caloric intake—appear to be more feasible targets for therapy. In particular, nitric oxide (NO) is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance. This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease.</p></abstract><kwd-group><kwd>nitric oxide</kwd><kwd>diabetes</kwd><kwd>insulin resistance</kwd><kwd>obesity</kwd><kwd>eNOS</kwd><kwd>mitochondria</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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