DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Y | ko |
dc.contributor.author | Naseem, RH | ko |
dc.contributor.author | Duplomb, L | ko |
dc.contributor.author | Park, BH | ko |
dc.contributor.author | Garry, DJ | ko |
dc.contributor.author | Richardson, JA | ko |
dc.contributor.author | Schaffer, JE | ko |
dc.contributor.author | Unger, RH | ko |
dc.date.accessioned | 2024-03-22T03:01:24Z | - |
dc.date.available | 2024-03-22T03:01:24Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2004-09 | - |
dc.identifier.citation | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.101, no.37, pp.13624 - 13629 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318668 | - |
dc.description.abstract | The physiologic function of the progressive hyperleptinemia of diet-induced obesity is unknown. However, that lipotoxicity in nonadipose tissues of congenitally unleptinized obese rodents is far greater than in hyperleptinemic diet-induced obesity rodents has suggested an antilipotoxic role. To test this hypothesis, mice with severe lipotoxic cardiomyopathy, induced transgenically by cardiomyocyte-specific overexpression of the acyl CoA synthase (ACS) gene, were made hyperleptinemic by treatment with recombinant adenovirus containing the leptin cDNA. Normoleptinemic control ACS-transgenic mice developed severe dilated cardiomyopathy with thickened left ventricular walls and profound impairment of systolic function on echocardiogram; histologically, there was severe myofiber disorganization and interstitial fibrosis, with intracytoplasmic lipid vacuoles identifiable by electron microscope. By contrast, the hearts of hyperleptinemic ACS-transgenic mice appeared normal, with normal echocardiograms and cardiac triglyceride (TG) contents. Their lower myocardial TG content was ascribed primarily to profound lowering of plasma TG and free fatty acids; free fatty acids were 17% of normal at 8 weeks. Additionally, enhanced myocardial AMP-activated protein kinase phosphorylation may have increased fatty acid oxidation, thereby contributing to the lowering of lipid stores. We conclude that obesity-level hyperleptinemia protects the heart from lipotoxicity. | - |
dc.language | English | - |
dc.publisher | NATL ACAD SCIENCES | - |
dc.title | Hyperleptinemia prevents lipotoxic cardiomyopathy in acyl CoA synthase transgenic mice | - |
dc.type | Article | - |
dc.identifier.wosid | 000223917900042 | - |
dc.identifier.scopusid | 2-s2.0-4544252278 | - |
dc.type.rims | ART | - |
dc.citation.volume | 101 | - |
dc.citation.issue | 37 | - |
dc.citation.beginningpage | 13624 | - |
dc.citation.endingpage | 13629 | - |
dc.citation.publicationname | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | - |
dc.identifier.doi | 10.1073/pnas.0405499101 | - |
dc.contributor.localauthor | Park, BH | - |
dc.contributor.nonIdAuthor | Lee, Y | - |
dc.contributor.nonIdAuthor | Naseem, RH | - |
dc.contributor.nonIdAuthor | Duplomb, L | - |
dc.contributor.nonIdAuthor | Garry, DJ | - |
dc.contributor.nonIdAuthor | Richardson, JA | - |
dc.contributor.nonIdAuthor | Schaffer, JE | - |
dc.contributor.nonIdAuthor | Unger, RH | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | leptin | - |
dc.subject.keywordAuthor | SIRT1 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | AMP-activated protein kinase | - |
dc.subject.keywordAuthor | triglycerides | - |
dc.subject.keywordPlus | FATTY-ACID OXIDATION | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | DIABETES-MELLITUS | - |
dc.subject.keywordPlus | WHITE ADIPOCYTES | - |
dc.subject.keywordPlus | MALONYL-COA | - |
dc.subject.keywordPlus | OBESE RATS | - |
dc.subject.keywordPlus | LEPTIN | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | MODEL | - |
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