Abstract
We investigated whether hyperbaric oxygen enhances the oxidative metabolic capacity of the skeletal muscle and attenuates adipocyte hypertrophy in type 2 diabetic rats with obesity. Five-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) and Long-Evans Tokushima Otsuka (LETO) rats were used as diabetic animals and nondiabetic controls, respectively, and assigned to control and hyperbaric oxygen groups. Animals in the hyperbaric oxygen group were exposed to an atmospheric pressure of 1.25 with an oxygen concentration of 36% for 3 h daily. The glucose level at 27 weeks of age was significantly higher in OLETF rats than in LETO rats, but the elevation was inhibited in OLETF rats exposed to hyperbaric oxygen. The slow-to-fast fiber transition in the skeletal muscle was observed in OLETF rats, but the shift was inhibited in OLETF rats exposed to hyperbaric oxygen. Additionally, the oxidative enzyme activity of muscle fibers was increased by hyperbaric oxygen. The adipocyte size was larger in OLETF rats than in LETO rats, but hypertrophied adipocytes were not observed in OLETF rats exposed to hyperbaric oxygen. Hyperbaric oxygen enhances glucose and lipid metabolism in the skeletal muscle, indicating that hyperbaric oxygen can prevent elevation of glucose and adipocyte hypertrophy in diabetic rats with obesity.
Highlights
Overeating and physical inactivity induce an increased energy intake and result in the enlargement of white adipocytes [1]
The present study revealed that hyperbaric oxygen enhances the oxidative metabolic capacity of skeletal muscles and attenuates adipocyte hypertrophy in type 2 diabetic animals with obesity
The fiber-type distribution was altered in the skeletal muscle, and elevation of glucose and adipocyte hypertrophy were observed in type 2 diabetic animals with obesity
Summary
Overeating and physical inactivity induce an increased energy intake and result in the enlargement of white adipocytes [1]. It is well known that hypertrophied adipocytes induce obesity and type 2 diabetes [2]. It has been suggested that hypertrophied adipocytes result in the overexpression of tumor necrosis factor-α, causing the insulin resistance that often accompanies obesity [3]. Hypertrophied adipocytes reduced the expression of adiponectin in obesity, which is associated with the subsequent development of type 2 diabetes [4]. A chronically high glucose level decreases insulin sensitivity in the skeletal muscle and causes insulin resistance [5]. Skeletal muscles that are affected by insulin resistance cannot adequately dispose glucose because of impaired insulin-stimulated glucose uptake in muscle fibers
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