Sex, sex steroids, and diabetic cardiomyopathy: making the case for experimental focus

Reichelt, Melissa E., Mellor, Kimberley M., Bell, James R., Chandramouli, Chanchal, Headrick, John P. and Delbridge, Lea M. D. (2013) Sex, sex steroids, and diabetic cardiomyopathy: making the case for experimental focus. American Journal of Physiology. Heart and Circulatory Physiology, 305 6: H779-H792. doi:10.1152/ajpheart.00141.2013


Author Reichelt, Melissa E.
Mellor, Kimberley M.
Bell, James R.
Chandramouli, Chanchal
Headrick, John P.
Delbridge, Lea M. D.
Title Sex, sex steroids, and diabetic cardiomyopathy: making the case for experimental focus
Journal name American Journal of Physiology. Heart and Circulatory Physiology   Check publisher's open access policy
ISSN 0363-6135
1522-1539
Publication date 2013-09-15
Year available 2013
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1152/ajpheart.00141.2013
Open Access Status Not yet assessed
Volume 305
Issue 6
Start page H779
End page H792
Total pages 14
Place of publication Bethesda, MD, United States
Publisher American Physiological Society
Language eng
Abstract More than three decades ago, the Framingham study revealed that cardiovascular risk is elevated for all diabetics and that this jeopardy is substantially accentuated for women in particular. Numerous studies have subsequently documented worsened cardiac outcomes for women. Given that estrogen and insulin exert major regulatory effects through common intracellular signaling pathways prominent in maintenance of cardiomyocyte function, a sex-hormone:diabetic-disease interaction is plausible. Underlying aspects of female cardiovascular pathophysiology that exaggerate cardiovascular diabetic risk may be identified, including increased vulnerability to coronary microvascular disease, age-dependent impairment of insulinsensitivity, and differential susceptibility to hyperglycemia. Since Framingham, considerable progress has been made in the development of experimental models of diabetic disease states, including a diversity of genetic rodent models. Ample evidence indicates that animal models of both type 1 and 2 diabetes variably recapitulate aspects of diabetic cardiomyopathy including diastolic and systolic dysfunction, and cardiac structural pathology including fibrosis, loss of compliance, and in some instances ventricular hypertrophy. Perplexingly, little of this work has explored the relevance and mechanisms of sexual dimorphism in diabetic cardiomyopathy. Only a small number of experimental studies have addressed this question, yet the prospects for gaining important mechanistic insights from further experimental enquiry are considerable. The case for experimental interrogation of sex differences, and of sex steroid influences in the aetiology of diabetic cardiomyopathy, is particularly compelling-providing incentive for future investigation with ultimate therapeutic potential.
Keyword Cardiac
Contractility
Diabetes
Gender
Hypertrophy
Insulin-sensitivity
Sex
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: School of Biomedical Sciences Publications
 
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