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Article: Generation and characterization of sodium-dicarboxylate cotransporter-deficient mice

TitleGeneration and characterization of sodium-dicarboxylate cotransporter-deficient mice
Authors
KeywordsCaloric restriction
Dicarboxylates
Gene knockout mice
NaDC1
Renal ischemia
Renal transporter
Issue Date2007
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2007, v. 72 n. 1, p. 63-71 How to Cite?
AbstractThe sodium-dependent dicarboxylate cotransporter (NaDC1) has a proposed function of reabsorbing various Krebs cycle intermediates in the kidney and the small intestine. Since Krebs cycle intermediates have been suggested to be important for renal cell survival and recovery after hypoxia and reoxygenation, the transporter may play a role in the recovery of the kidney. Additionally, mutations in the transporter homolog in Drosophila led to fly longevity which was thought to be similar to that induced by caloric restriction (CR). To clarify the role of the sodium dicarboxylate cotransporter in vivo we generated cotransporter-deficient mice. These knockout mice excreted significantly higher amounts of various Krebs cycle intermediates in their urine; thus confirming the proposed function to reabsorb these metabolic intermediates in the kidney. No other phenotypic change was identified in these mice, however. Transporter deficiency did not affect renal function under normal physiological conditions, nor did it have an effect on renal damage and recovery from ischemic injury. Additionally, the absence of the transporter did not lead to metabolic or physiological changes associated with CR. Our results suggest that although the sodium dicarboxylate cotransporter is involved in regulating levels of various Krebs cycle intermediates in the kidney, impaired uptake of these intermediates does not significantly affect renal function under normal or ischemic stress. © 2007 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/67619
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, HTBen_HK
dc.contributor.authorKo, BCBen_HK
dc.contributor.authorCheung, AKHen_HK
dc.contributor.authorLam, AKMen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T05:56:44Z-
dc.date.available2010-09-06T05:56:44Z-
dc.date.issued2007en_HK
dc.identifier.citationKidney International, 2007, v. 72 n. 1, p. 63-71en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67619-
dc.description.abstractThe sodium-dependent dicarboxylate cotransporter (NaDC1) has a proposed function of reabsorbing various Krebs cycle intermediates in the kidney and the small intestine. Since Krebs cycle intermediates have been suggested to be important for renal cell survival and recovery after hypoxia and reoxygenation, the transporter may play a role in the recovery of the kidney. Additionally, mutations in the transporter homolog in Drosophila led to fly longevity which was thought to be similar to that induced by caloric restriction (CR). To clarify the role of the sodium dicarboxylate cotransporter in vivo we generated cotransporter-deficient mice. These knockout mice excreted significantly higher amounts of various Krebs cycle intermediates in their urine; thus confirming the proposed function to reabsorb these metabolic intermediates in the kidney. No other phenotypic change was identified in these mice, however. Transporter deficiency did not affect renal function under normal physiological conditions, nor did it have an effect on renal damage and recovery from ischemic injury. Additionally, the absence of the transporter did not lead to metabolic or physiological changes associated with CR. Our results suggest that although the sodium dicarboxylate cotransporter is involved in regulating levels of various Krebs cycle intermediates in the kidney, impaired uptake of these intermediates does not significantly affect renal function under normal or ischemic stress. © 2007 International Society of Nephrology.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectCaloric restrictionen_HK
dc.subjectDicarboxylatesen_HK
dc.subjectGene knockout miceen_HK
dc.subjectNaDC1en_HK
dc.subjectRenal ischemiaen_HK
dc.subjectRenal transporteren_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - physiologyen_HK
dc.subject.meshCaloric Restrictionen_HK
dc.subject.meshCell Differentiation - physiologyen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCitrates - blooden_HK
dc.subject.meshCitric Acid Cycle - physiologyen_HK
dc.subject.meshCreatinine - blooden_HK
dc.subject.meshDicarboxylic Acid Transporters - genetics - physiologyen_HK
dc.subject.meshKidney - pathology - physiology - physiopathologyen_HK
dc.subject.meshKidney Tubules, Proximal - pathology - physiology - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshOrganic Anion Transporters, Sodium-Dependent - genetics - physiologyen_HK
dc.subject.meshReperfusion Injury - pathology - physiopathologyen_HK
dc.subject.meshSymporters - genetics - physiologyen_HK
dc.titleGeneration and characterization of sodium-dicarboxylate cotransporter-deficient miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=72&spage=63&epage=71&date=2007&atitle=Generation+and+characterization+of+sodium-dicarboxylate+cotransporter-deficient+miceen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.ki.5002258en_HK
dc.identifier.pmid17410095-
dc.identifier.scopuseid_2-s2.0-34347344988en_HK
dc.identifier.hkuros132270en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34347344988&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume72en_HK
dc.identifier.issue1en_HK
dc.identifier.spage63en_HK
dc.identifier.epage71en_HK
dc.identifier.isiWOS:000247909800010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.f10001089862-
dc.identifier.scopusauthoridHo, HTB=55202560700en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK
dc.identifier.scopusauthoridCheung, AKH=7401806412en_HK
dc.identifier.scopusauthoridLam, AKM=7201848036en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.citeulike3129673-

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