Abstract
Physical activity exerts positive effects on glycemic control in type 2 diabetes (T2D), which is mediated in part by extensive metabolic and molecular remodeling of skeletal muscle in response to exercise, while many regulators of skeletal muscle remain unclear. In the present study, we investigated the effects of acute exercise on skeletal muscle transcriptomic responses in the Goto-Kakizaki (GK) rats which can spontaneously develop T2D. The transcriptomes of skeletal muscle from both 8-week-old GK and Wistar rats that underwent a single exercise session (60 min running using an animal treadmill at 15 m/min) or remained sedentary were analyzed by next-generation RNA sequencing. We identified 819 differentially expressed genes in the sedentary GK rats compared with those of the sedentary Wistar rats. After a single bout of running, we found 291 and 598 genes that were differentially expressed in the exercise GK and exercise Wistar rats when compared with the corresponding sedentary rats. By integrating our data and previous studies including RNA or protein expression patterns and transgenic experiments, the downregulated expression of Fasn and upregulated expression of Tbc1d1, Hk2, Lpin1, Ppargc1a, Sorbs1, and Hmox1 might enhance glucose uptake or improve insulin sensitivity to ameliorate hyperglycemia in the exercise GK rats. Our results provide mechanistic insight into the beneficial effects of exercise on hyperglycemia and insulin action in skeletal muscle of diabetic GK rats.
Highlights
Diabetes has become a growing global public health problem, leading to millions of deaths and considerable healthcare expenditure (Da et al, 2016)
Skeletal muscle plays an important role in maintaining systemic glucose homeostasis because it is one of the primary organs for glucose metabolism
Substantial evidence indicated that physical activity plays an essential role in the prevention and treatment of type 2 diabetes (T2D) and even a single bout of exercise can improve hyperglycemia and insulin resistance (Colberg et al, 2010; Richter and Hargreaves, 2013)
Summary
Diabetes has become a growing global public health problem, leading to millions of deaths and considerable healthcare expenditure (Da et al, 2016). According to the International Diabetes Federation (IDF), 451 million people were estimated to have diabetes worldwide in 2017, with a projected increase to 693 million people by 2045 (Cho et al, 2018). Among these patients, 87– 91% suffered from type 2 diabetes (T2D) which is characterized by hyperglycemia and insulin resistance in target organs (Chatterjee et al, 2017). The prevalence of T2D in Asian populations has increased rapidly, with more than 60% of global T2D cases occurred in Asia. Suitable animal models are needed to study the pathophysiology and treatments of non-obese T2D patients
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