The impact of a 12-week high-fructose diet on the metabolic syndrome and ischaemia-reperfusion injury in rats
Abstract
Excess fructose consumption is implicated globally in metabolic pathologies, ultimately resulting in cardiac mortality. As such, robust animal models of fructose-induced pathology, with a cardiac phenotype, are required to investigate underlying disease processes. We evaluated the impact of a 12-week high-fructose diet on cardiometabolic parameters and susceptibility to ischaemia–reperfusion injury in Wistar rats. Our protocol demonstrated increased fructose intake and systemic exposure, accompanied by enlargement of the liver and renal hypertrophy. Despite this, functional cardiac impairment was not demonstrated via echocardiographic assessment of systolic or diastolic function. In addition, increased dietary fructose exposure was not associated with increased susceptibility to ischaemia-reperfusion injury in an ex vivo Langendorff model of global ischaemia, and no gross inflammatory or fibrotic changes were evident on histological examination. Explanations for the lack of observed cardiac phenotype may include the necessity of additional physiological stressors e.g. high fat or salt intake as well as the presence of an active uricase enzyme in rodents. These considerations could explain the heterogeneity of outcomes observed in available animal models and the disparity with human observational data, where the negative impacts impact of increased dietary fructose intake are readily observed.
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BibTeX
@article{mathew2026impact,
title = {{The impact of a 12-week high-fructose diet on the metabolic syndrome and ischaemia-reperfusion injury in rats}},
author = {David C. Mathew and Siavash Beikoghli-Kalkhoran and Alan D. Salama and Sean M. Davidson and Derek M. Yellon},
journal = {Scientific Reports},
year = {2026},
month = oct,
doi = {10.1038/s41598-026-73467-x},
url = {https://www.nature.com/articles/s41598-026-73467-x},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The impact of a 12-week high-fructose diet on the metabolic syndrome and ischaemia-reperfusion injury in rats
AU - David C. Mathew
AU - Siavash Beikoghli-Kalkhoran
AU - Alan D. Salama
AU - Sean M. Davidson
AU - Derek M. Yellon
PY - 2026
DA - 2026/10/03
JO - Scientific Reports
DO - 10.1038/s41598-026-73467-x
UR - https://www.nature.com/articles/s41598-026-73467-x
AB - Excess fructose consumption is implicated globally in metabolic pathologies, ultimately resulting in cardiac mortality. As such, robust animal models of fructose-induced pathology, with a cardiac phenotype, are required to investigate underlying disease processes. We evaluated the impact of a 12-week high-fructose diet on cardiometabolic parameters and susceptibility to ischaemia–reperfusion injury in Wistar rats. Our protocol demonstrated increased fructose intake and systemic exposure, accompanied by enlargement of the liver and renal hypertrophy. Despite this, functional cardiac impairment was not demonstrated via echocardiographic assessment of systolic or diastolic function. In addition, increased dietary fructose exposure was not associated with increased susceptibility to ischaemia-reperfusion injury in an ex vivo Langendorff model of global ischaemia, and no gross inflammatory or fibrotic changes were evident on histological examination. Explanations for the lack of observed cardiac phenotype may include the necessity of additional physiological stressors e.g. high fat or salt intake as well as the presence of an active uricase enzyme in rodents. These considerations could explain the heterogeneity of outcomes observed in available animal models and the disparity with human observational data, where the negative impacts impact of increased dietary fructose intake are readily observed.
SN - 2045-2322
ER -