ArticleIranian journal of medical sciences2026
Inflammasome Suppression via Combined Training Modulates Downstream Cytokines (Interleukin-1β/Caspase-1) and Improves Insulin Resistance in Diabetic Rats.
Article in Iranian journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Diabetic Cardiomyopathy (DCM) is connected to prolonged systemic glucose metabolism and/or hyperinsulinemia-induced cardiac metaflammation. This study aims to investigate the effects of combined endurance and resistance training on the protein levels of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), caspase-1, and interleukin -1β (IL-1β) in the myocardium of male rats with type 2 diabetes. Methods: In this experimental study, 24 male Wistar rats (8 weeks old, 260±20 g) were randomly divided into three groups: (n=8/groups): Normal Control (NC), Diabetes Control (DC), and Diabetes+Combined Training (DCT). After type 2 diabetes induction, the training group performed the combined training for 8 weeks, five sessions/week, in spring 2024 at AJA University of Medical Sciences. Approximately 48 hours following the end of the training protocol, blood samples and myocardium tissue were taken for subsequent assessment of inflammatory and biochemical markers. Group comparisons were achieved using one-way ANOVA, followed by the Tukey Results: Chronic implementation of combined training significantly downregulated final weight (P=0.033), protein levels of NLRP3, Caspase-1, and IL-1β (P=0.03, 0.001 and 0.019, respectively) in the cardiac tissue as well as modulation the homeostatic model assessment for insulin resistance (HOMA-IR: P=0.039) via attenuation of serum glucose and insulin levels (P=0.032 and 0.07) of the training group compared to the diabetic group. Conclusion: The modality of combined training (endurance+resistance) can reduce the risk factors associated with DCM in the myocardium of type 2 diabetic rats.
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