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dc.contributor.authorChandramouli, C
dc.contributor.authorReichelt, ME
dc.contributor.authorCurl, CL
dc.contributor.authorVarma, U
dc.contributor.authorBienvenu, LA
dc.contributor.authorKoutsifeli, P
dc.contributor.authorRaaijmakers, AJA
dc.contributor.authorDe Blasio, MJ
dc.contributor.authorQin, CX
dc.contributor.authorJenkins, AJ
dc.contributor.authorRitchie, RH
dc.contributor.authorMellor, KM
dc.contributor.authorDelbridge, LMD
dc.date.accessioned2020-12-18T03:42:29Z
dc.date.available2020-12-18T03:42:29Z
dc.date.issued2018-02-05
dc.identifierpii: 10.1038/s41598-018-20703-8
dc.identifier.citationChandramouli, C., Reichelt, M. E., Curl, C. L., Varma, U., Bienvenu, L. A., Koutsifeli, P., Raaijmakers, A. J. A., De Blasio, M. J., Qin, C. X., Jenkins, A. J., Ritchie, R. H., Mellor, K. M. & Delbridge, L. M. D. (2018). Diastolic dysfunction is more apparent in STZ-induced diabetic female mice, despite less pronounced hyperglycemia. SCIENTIFIC REPORTS, 8 (1), https://doi.org/10.1038/s41598-018-20703-8.
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/11343/255886
dc.description.abstractDiabetic cardiomyopathy is a distinct pathology characterized by early emergence of diastolic dysfunction. Increased cardiovascular risk associated with diabetes is more marked for women, but an understanding of the role of diastolic dysfunction in female susceptibility to diabetic cardiomyopathy is lacking. To investigate the sex-specific relationship between systemic diabetic status and in vivo occurrence of diastolic dysfunction, diabetes was induced in male and female mice by streptozotocin (5x daily i.p. 55 mg/kg). Echocardiography was performed at 7 weeks post-diabetes induction, cardiac collagen content assessed by picrosirius red staining, and gene expression measured using qPCR. The extent of diabetes-associated hyperglycemia was more marked in males than females (males: 25.8 ± 1.2 vs 9.1 ± 0.4 mM; females: 13.5 ± 1.5 vs 8.4 ± 0.4 mM, p < 0.05) yet in vivo diastolic dysfunction was evident in female (E/E' 54% increase, p < 0.05) but not male diabetic mice. Cardiac structural abnormalities (left ventricular wall thinning, collagen deposition) were similar in male and female diabetic mice. Female-specific gene expression changes in glucose metabolic and autophagy-related genes were evident. This study demonstrates that STZ-induced diabetic female mice exhibit a heightened susceptibility to diastolic dysfunction, despite exhibiting a lower extent of hyperglycemia than male mice. These findings highlight the importance of early echocardiographic screening of asymptomatic prediabetic at-risk patients.
dc.languageEnglish
dc.publisherNATURE PUBLISHING GROUP
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleDiastolic dysfunction is more apparent in STZ-induced diabetic female mice, despite less pronounced hyperglycemia
dc.typeJournal Article
dc.identifier.doi10.1038/s41598-018-20703-8
melbourne.affiliation.departmentSchool of BioSciences
melbourne.affiliation.departmentAnatomy and Neuroscience
melbourne.affiliation.departmentPhysiology
melbourne.affiliation.departmentBiochemistry and Pharmacology
melbourne.affiliation.departmentMedicine (St Vincent's)
melbourne.affiliation.departmentMelbourne Medical School
melbourne.affiliation.facultyScience
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titleScientific Reports
melbourne.source.volume8
melbourne.source.issue1
melbourne.identifier.nhmrc628841
melbourne.identifier.nhmrc1027865
dc.rights.licenseCC BY
melbourne.elementsid1305450
melbourne.contributor.authorVarma, Upasna
melbourne.contributor.authorCurl, Claire
melbourne.contributor.authorMellor, Kimberley
melbourne.contributor.authorDelbridge, Leanne
melbourne.contributor.authorde Blasio, Miles
melbourne.contributor.authorBienvenu, Laura
melbourne.contributor.authorQin, Chengxue
melbourne.contributor.authorJenkins, Alicia
melbourne.contributor.authorRitchie, Rebecca
dc.identifier.eissn2045-2322
melbourne.identifier.fundernameidNHMRC, 628841
melbourne.identifier.fundernameidNHMRC, 1027865
melbourne.accessrightsOpen Access


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