Journal article

A high-sucrose diet exacerbates the left ventricular phenotype in a high fat-fed streptozotocin rat model of diabetic cardiomyopathy

A Velagic, M Li, M Deo, JC Li, H Kiriazis, DG Donner, D Anderson, MJ De Blasio, OL Woodman, BK Kemp-Harper, CX Qin, RH Ritchie

American Journal of Physiology Heart and Circulatory Physiology | Published : 2023

Abstract

Left ventricular (LV) dysfunction is an early, clinically detectable sign of cardiomyopathy in type 2 diabetes mellitus (T2DM) that precedes the development of symptomatic heart failure. Preclinical models of diabetic cardiomyopathy are essential to develop therapies that may prevent or delay the progression of heart failure. This study examined the molecular, structural, and functional cardiac phenotype of two rat models of T2DM induced by a high-fat diet (HFD) with a moderate- or high-sucrose content (containing 88.9 or 346 g/kg sucrose, respectively), plus administration of low-dose streptozotocin (STZ). At 8 wk of age, male Sprague–Dawley rats commenced a moderate- or high-sucrose HFD. T..

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Grants

Awarded by Diabetes Australia Research Trust


Funding Acknowledgements

This study was funded in part by Diabetes Australia Research Trust Grant Y13M1-RITR (to R.H.R. and B.K.K.-H.) , National Health and Medical Research Council (NHMRC) of Australia Project Grants ID1120859 (to R.H.R. and B.K.K.-H.) , and the Victorian Government of Australia's Operational Infrastructure Support Program. R.H.R. was supported by an NHMRC Senior Research Fellowship ID1059960. C.X.Q. is supported by a National Heart Foundation of Australia Future Leader Fellowship. A.V. is supported by a Research Training Program (RTP) Scholarship and a Monash Graduate Excellence Scholarship provided by Monash University. M.L. is supported by an RTP Scholarship provided by Monash University.