Abstract
Regular exercise plays an important role in the prevention and treatment of type 2 diabetes (T2D). The synthesis and secretion of myokines in response to contraction may contribute to the beneficial metabolic effects of exercise. However, some exercise‐induced responses may be attenuated in T2D. Here, we investigated whether the effect of acute exercise on selected myokines are impaired in T2D. Skeletal muscle biopsies and blood samples were obtained from 13 men with T2D and 14 weight‐matched, glucose‐tolerant men before, immediately after and 3‐h after acute exercise (60 min cycling) to examine muscle expression and plasma/serum levels of selected myokines. One‐hour of exercise increased muscle expression of IL6, FGF21, ANGPTL4, CHI3L1, CTGF and CYR61, of which FGF21, ANGPTL4 and CHI3L1 increased further 3‐h into recovery, whereas expression of IL6, CYR61, and CTGF returned to baseline levels. There was no immediate effect of exercise on IL15 expression, but it decreased 3‐h into recovery. Plasma IL‐6 increased robustly, whereas circulating levels of FGF21, ANGPTL4, IL‐15, and CHI3L1 increased only modestly in response to exercise. All returned toward baseline levels 3‐h into recovery except for plasma ANGPTL4, which increased further. No significant differences in these responses to exercise were observed between the groups. Our results demonstrate that muscle expression and circulating levels of selected known and putative myokines were equally regulated by acute exercise in patients with T2D and weight‐matched controls. This suggests that the potential beneficial metabolic effects of these myokines are not impaired in patients with T2D.
Highlights
Insulin resistance is an important hallmark in the pathogenesis of type 2 diabetes (T2D)
Our results demonstrate that muscle expression and circulating levels of selected known and putative myokines were regulated by acute exercise in patients with T2D and weight-matched controls
Muscle expression of IL15 did not change in response to acute exercise, but decreased slightly 3-h into recovery in both groups compared with basal levels (P < 0.001) and immediately after exercise (P < 0.001) (Fig. 1C)
Summary
Insulin resistance is an important hallmark in the pathogenesis of type 2 diabetes (T2D). Exercise is associated with numerous beneficial metabolic effects including improved maximal pulmonary oxygen uptake (VO2max), insulin sensitivity, and whole-body glucose and lipid metabolism (Hawley 2004; Hawley et al 2014). Regular exercise activates various key metabolic pathways leading to enhanced abundance of proteins involved in insulin-signaling, lipid and glucose metabolism, and mitochondrial oxidative metabolism (Egan and Zierath 2013). Some studies have reported attenuated exercise-mediated increases in insulin sensitivity, VO2max and muscle expression of markers of mitochondrial oxidative metabolism in individuals with prediabetes and T2D indicating the existence of exercise resistance (De Filippis et al 2008; Hernandez-Alvarez et al 2010; Stephens and Sparks 2015). To what extent production and release of myokines from skeletal muscle in response to acute exercise are impaired in patients with T2D remains to be established
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