Greater hyperthermia in men with type 2 diabetes does not lead to higher serum levels of cellular stress biomarkers following exercise-heat stress.

Nicholas Goulet, Emily J Tetzlaff, James J McCormick, Kelli E King, Kristina-Marie T Janetos, Ronald J Sigal, Pierre Boulay, Glen P Kenny
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Abstract

Type 2 diabetes (T2D) is associated with worsening age-related impairments in heat loss, causing higher core temperature during exercise. We evaluated whether these thermoregulatory impairments occur with altered serum protein responses to heat stress by measuring cytoprotection, inflammation, and tissue damage biomarkers in middle-aged-to-older men (50-74 years) with (n = 16) and without (n = 14) T2D following exercise in 40°C. There were no changes in irisin, klotho, HSP70, sCD14, TNF-α, and IL-6, whereas NGAL (+539 pg/mL, p = 0.002) and iFABP (+250 pg/mL, p < 0.001) increased similarly across groups. These similar response patterns occurred despite elevated core temperature in individuals with T2D, suggesting greater heat vulnerability.

2型糖尿病男性患者在运动热应激后,更高的热应激并不会导致血清中细胞应激生物标志物水平升高。
2 型糖尿病(T2D)与年龄相关的散热障碍恶化有关,会导致运动时核心温度升高。我们通过测量患有(n=16)和不患有(n=14)T2D 的中老年男性(50-74 岁)在 40°C 下运动后的细胞保护、炎症和组织损伤生物标志物,评估了这些体温调节障碍是否与血清蛋白对热应激反应的改变有关。鸢尾素、klotho、HSP70、sCD14、TNF-α和IL-6没有变化,而NGAL(+539 pg/mL,p=0.002)和iFABP(+250 pg/mL,p=0.003)则发生了变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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