Key result
A 6-week aerobic exercise regimen significantly reduced cardiac inflammatory biomarkers, including PKR gene expression (P ≤ 0.01), in rats with high-fat/fructose diet-induced obesity.
Why the study?
Obesity directly contributes to cardiovascular risk factors, motivating an investigation into how aerobic training impacts cardiac biomarkers via PKR/TLR gene expression in high-fat/fructose diet-induced obesity.
Does aerobic exercise improve cardiac inflammatory biomarkers and regulate the PKR/TLR pathway in an obese rat model?
Does aerobic exercise improve cardiac inflammatory biomarkers and regulate the PKR/TLR pathway in an obese rat model?
p-value: p=≤0.01
Aerobic exercise improves cardiovascular inflammatory biomarkers and downregulates the PKR/TLR pathway in a high-fat/fructose diet-induced obese rat model.
Aerobic exercise may attenuate obesity-related cardiac inflammation in rats; hypothesis-generating for PKR/TLR modulation in humans, should not change practice.
Background: Obesity is a direct contributor to cardiovascular risk factors such as diabetes, high blood pressure, and cardiac failure. Objectives: The goal of this study was to examine how aerobic training impacts cardiac biomarkers by analyzing the protein kinase R (PKR)/toll-like receptor (TLR) gene expression in an obesity model induced by a high-fat/fructose diet. Methods: In this study, we used 24 Wistar rats with a weight range of 204 ± 11.3 grams. They were divided into three groups: A standard diet group, a high-fat diet (HFD) with fructose group (60% fat and 25% fructose), and an obese rats group with aerobic exercise. At the end of the study, the Neutrophil/lymphocyte ratio, lipoprotein-associated phospholipase A (Lp-PLA2), cystatin C, and PKR/TLR gene expression were measured in all groups. Results: Compared to the control group, the HFD with fructose increased the Neutrophil/lymphocyte ratio, Lp-PLA2, and cystatin C. The expression levels of TLR (P ≤ 0.001) and PKR (P ≤ 0.01) genes in the cardiac tissue of obese rats were significantly higher than those in the control group. The obese rats showed a significant decrease in PKR gene expression when following the high-fat/fructose diet plus aerobic exercise regimen. However, the obese group did not exhibit a significant difference in TLR4 gene expression compared to the HFD plus aerobic exercise rats. Conclusions: Based on the data, aerobic exercise was found to affect the PKR/TLR pathway, leading to improved cardiovascular inflammatory biomarkers in obese rats.
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Mahmmodi et al. (2024) studied Obesity-induced cardiac inflammation (n=24). Aerobic exercise vs. High-fat/fructose diet without exercise and standard diet was evaluated on PKR gene expression in cardiac tissue (p=≤0.01). A 6-week aerobic exercise regimen significantly reduced cardiac inflammatory biomarkers, including PKR gene expression (P ≤ 0.01), in rats with high-fat/fructose diet-induced obesity.
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