Key result
A high-fructose diet in hypertriglyceridemic rats significantly decreased the threshold for inducing ventricular fibrillation to 18.81 mA compared to 29.10 mA in controls.
Why the study?
High-fructose intake worsens metabolic and cardiovascular health, but the precise mechanisms and its impact on heart function in metabolic syndrome remain unclear.
Does a high-fructose diet worsen ex vivo heart function and increase arrhythmia susceptibility in hypertriglyceridemic rats?
Does a high-fructose diet worsen ex vivo heart function and increase arrhythmia susceptibility in hypertriglyceridemic rats?
In a rat model of metabolic syndrome, a high-fructose diet exacerbated dyslipidemia and increased susceptibility to life-threatening ventricular arrhythmias during ischemia/reperfusion.
Answers are grounded in this paper and cite their sources.
High-fructose intake may increase reperfusion VF risk in metabolic syndrome; hypothesis-generating for human arrhythmia prevention.
A high-fructose intake (HFI) in food, sweetened beverages, and soft drinks appears to be one of the risk factors that worsens human metabolic and cardiovascular health, although the more accurate mechanism remains unclear. Hypertriglyceridemic (HTG) rats represent a suitable animal model of metabolic syndrome where the consumption of an HFI could have an additional aggravating impact. We aimed to study the effect of fructose on the heart functions. Male HTG rats had HFI or a standard diet for five weeks. Heart function was tested ex vivo on the perfused heart using the Langendorff technique. Isolated hearts underwent 25 min ischemia (I) and 30 min reperfusion (R). Left ventricular developed pressure (LVDP), ventricular premature beats, and dysrhythmias were monitored during R. At the end of the R, ventricular fibrillation (VF) was evoked electrically. Systolic blood pressure, glucose level, serum total cholesterol (TC), triglycerides (TAG), and thiobarbituric acid reactive substances (TBARS) in the kidney were determined. The LVDP showed a reduced return to the input values, the duration of VF in R increased, and the threshold for VF induction decreased. Serum TC, TAG, and kidney TBARS were increased. The effect of HFI on heart ventricular impairment was associated with the reduced threshold for induction of VF and aggravated dyslipidemia. The results point to the adverse impact of dietary high-fructose intake in rats with hypertriglyceridemia.
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Knezl et al. (2024) studied Hypertriglyceridemia (n=28). High-fructose diet vs. Standard diet was evaluated on Ventricular fibrillation stimulation threshold (p=≤0.05). A high-fructose diet in hypertriglyceridemic rats significantly decreased the threshold for inducing ventricular fibrillation to 18.81 mA compared to 29.10 mA in controls.
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