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      Effects of Hyperbaric Oxygen on Metabolic Capacity of the Skeletal Muscle in Type 2 Diabetic Rats with Obesity

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          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.

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          Skeletal muscle lipid content and oxidative enzyme activity in relation to muscle fiber type in type 2 diabetes and obesity.

          S. Watkins, Johnny He, K. D. Kelley (2001)
          In obesity and type 2 diabetes, skeletal muscle has been observed to have a reduced oxidative enzyme activity, increased glycolytic activity, and increased lipid content. These metabolic characteristics are related to insulin resistance of skeletal muscle and are factors potentially related to muscle fiber type. The current study was undertaken to examine the interactions of muscle fiber type in relation to oxidative enzyme activity, glycolytic enzyme activity, and muscle lipid content in obese and type 2 diabetic subjects compared with lean healthy volunteers. The method of single-fiber analysis was used on vastus lateralis muscle obtained by percutaneous biopsy from 22 lean, 20 obese, and 20 type 2 diabetic subjects (ages 35+/-1, 42+/-2, and 52+/-2 years, respectively), with values for BMI that were similar in obese and diabetic subjects (23.7+/-0.7, 33.2+/-0.8, and 31.8+/-0.8 kg/m2, respectively). Oxidative enzyme activity followed the order of type I > type IIa > type IIb, but within each fiber type, skeletal muscle from obese and type 2 diabetic subjects had lower oxidative enzyme activity than muscle from lean subjects (P < 0.01). Muscle lipid content followed a similar pattern in relation to fiber type, and within each fiber type, muscle from obese and type 2 diabetic subjects had greater lipid content (P < 0.01). In summary, based on single-fiber analysis, skeletal muscle in obese and type 2 diabetic subjects mani-fests disturbances of oxidative enzyme activity and increased lipid content that are independent of the effect of fiber type.
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            Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance.

            Miroslaw Dudek, John P. Thyfault, Steven L. Britton … (2007)
            Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.
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              Reversal of diet-induced insulin resistance with a single bout of exercise in the rat: the role of PTP1B and IRS-1 serine phosphorylation.

              Maria Fernanda de A Fernandes, Patrícia Prada, M Velloso … (2006)
              Lifestyle interventions including exercise programmes are cornerstones in the prevention of obesity-related diabetes. In this study, we demonstrate that a single bout of exercise inhibits high-fat diet-induced insulin resistance. Diet-induced obesity (DIO) increased the expression and activity of the protein tyrosine phosphatase 1B (PTP1B) and attenuated insulin signalling in gastrocnemius muscle of rats, a phenomenon which was reversed by a single session of exercise. In addition, DIO was observed to lead to serine phosphorylation of insulin receptor substrate 1 (IRS-1), which was also reversed by exercise in muscle in parallel with a reduction in c-Jun N-terminal kinase (JNK) activity. Thus, acute exercise increased the insulin sensitivity during high-fat feeding in obese rats. Overall, these results provide new insights into the mechanism by which exercise restores insulin sensitivity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): ScientificWorldJournal
                Journal ID (iso-abbrev): ScientificWorldJournal
                Journal ID (publisher-id): TSWJ
                Title: The Scientific World Journal
                Publisher: The Scientific World Journal
                ISSN (Electronic): 1537-744X
                Publication date Collection: 2012
                Publication date (Electronic): 18 June 2012
                Volume: 2012
                Electronic Location Identifier: 637978
                Affiliations
                1Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe 654-0142, Japan
                2Laboratory of Cell Biology and Life Science, Graduate School of Human and Environmental Studies, Kyoto University, Yoshida-Nihonmatsu-cho, Sakyo-ku, Kyoto 606-8501, Japan
                3Department of Physical Therapy, Himeji Dokkyo University, 7-2-1 Kamiohno, Himeji 670-8524, Japan
                4Department of Food Sciences and Nutrition, Nagoya Women's University, 3-40 Shioji-cho, Mizuho-ku, Nagoya 467-8610, Japan
                Author notes

                Academic Editors: M. Diksic and G. J. Hausman

                Article
                DOI: 10.1100/2012/637978
                PMC ID: 3385605
                PubMed ID: 22778702
                SO-VID: 08a85fc3-6502-444e-936a-be4b09358172
                Copyright © Copyright © 2012 Naoto Fujita et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 31 March 2012
                Date accepted : 18 April 2012
                Categories
                Subject: Research Article

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