Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model.
<h4>Aims/hypothesis</h4>Diabetic voiding dysfunction has been reported in epidemiological dimension of individuals with diabetes mellitus. Animal models might provide new insights into the molecular mechanisms of this dysfunction to facilitate early diagnosis and to identify new drug tar...
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2013
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oai:doaj.org-article:03ae5072796f4b75b47c77d8ec5c938e2021-11-18T07:40:28ZMolecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model.1932-620310.1371/journal.pone.0066636https://doaj.org/article/03ae5072796f4b75b47c77d8ec5c938e2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23826106/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aims/hypothesis</h4>Diabetic voiding dysfunction has been reported in epidemiological dimension of individuals with diabetes mellitus. Animal models might provide new insights into the molecular mechanisms of this dysfunction to facilitate early diagnosis and to identify new drug targets for therapeutic interventions.<h4>Methods</h4>Thirty male Sprague-Dawley rats received either chow or high-fat diet for eleven weeks. Proteomic alterations were comparatively monitored in both groups to discover a molecular fingerprinting of the urinary bladder remodelling/dysfunction. Results were validated by ELISA, Western blotting and immunohistology.<h4>Results</h4>In the proteome analysis 383 proteins were identified and canonical pathway analysis revealed a significant up-regulation of acute phase reaction, hypoxia, glycolysis, β-oxidation, and proteins related to mitochondrial dysfunction in high-fat diet rats. In contrast, calcium signalling, cytoskeletal proteins, calpain, 14-3-3η and eNOS signalling were down-regulated in this group. Interestingly, we found increased ubiquitin proteasome activity in the high-fat diet group that might explain the significant down-regulation of eNOS, 14-3-3η and calpain.<h4>Conclusions/interpretation</h4>Thus, high-fat diet is sufficient to induce significant remodelling of the urinary bladder and alterations of the molecular fingerprint. Our findings give new insights into obesity related bladder dysfunction and identified proteins that may indicate novel pathophysiological mechanisms and therefore constitute new drug targets.Andreas OberbachNico JehmlichNadine SchlichtingMarco HeinrichStefanie LehmannHenry WirthHolger TillJens-Uwe StolzenburgUwe VölkerVolker AdamsJochen NeuhausPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e66636 (2013) |
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EN |
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Medicine R Science Q |
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Medicine R Science Q Andreas Oberbach Nico Jehmlich Nadine Schlichting Marco Heinrich Stefanie Lehmann Henry Wirth Holger Till Jens-Uwe Stolzenburg Uwe Völker Volker Adams Jochen Neuhaus Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| description |
<h4>Aims/hypothesis</h4>Diabetic voiding dysfunction has been reported in epidemiological dimension of individuals with diabetes mellitus. Animal models might provide new insights into the molecular mechanisms of this dysfunction to facilitate early diagnosis and to identify new drug targets for therapeutic interventions.<h4>Methods</h4>Thirty male Sprague-Dawley rats received either chow or high-fat diet for eleven weeks. Proteomic alterations were comparatively monitored in both groups to discover a molecular fingerprinting of the urinary bladder remodelling/dysfunction. Results were validated by ELISA, Western blotting and immunohistology.<h4>Results</h4>In the proteome analysis 383 proteins were identified and canonical pathway analysis revealed a significant up-regulation of acute phase reaction, hypoxia, glycolysis, β-oxidation, and proteins related to mitochondrial dysfunction in high-fat diet rats. In contrast, calcium signalling, cytoskeletal proteins, calpain, 14-3-3η and eNOS signalling were down-regulated in this group. Interestingly, we found increased ubiquitin proteasome activity in the high-fat diet group that might explain the significant down-regulation of eNOS, 14-3-3η and calpain.<h4>Conclusions/interpretation</h4>Thus, high-fat diet is sufficient to induce significant remodelling of the urinary bladder and alterations of the molecular fingerprint. Our findings give new insights into obesity related bladder dysfunction and identified proteins that may indicate novel pathophysiological mechanisms and therefore constitute new drug targets. |
| format |
article |
| author |
Andreas Oberbach Nico Jehmlich Nadine Schlichting Marco Heinrich Stefanie Lehmann Henry Wirth Holger Till Jens-Uwe Stolzenburg Uwe Völker Volker Adams Jochen Neuhaus |
| author_facet |
Andreas Oberbach Nico Jehmlich Nadine Schlichting Marco Heinrich Stefanie Lehmann Henry Wirth Holger Till Jens-Uwe Stolzenburg Uwe Völker Volker Adams Jochen Neuhaus |
| author_sort |
Andreas Oberbach |
| title |
Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| title_short |
Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| title_full |
Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| title_fullStr |
Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| title_full_unstemmed |
Molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| title_sort |
molecular fingerprint of high fat diet induced urinary bladder metabolic dysfunction in a rat model. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2013 |
| url |
https://doaj.org/article/03ae5072796f4b75b47c77d8ec5c938e |
| work_keys_str_mv |
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