Applied Biochemistry and Biotechnology

, Volume 179, Issue 5, pp 819–829 | Cite as

Whole Body Vibration Improves Insulin Resistance in db/db Mice: Amelioration of Lipid Accumulation and Oxidative Stress

  • Ying Liu
  • Mingming Zhai
  • Fan Guo
  • Tengrui Shi
  • Jiangzheng Liu
  • Xin Wang
  • Xiaodi Zhang
  • Da JingEmail author
  • Chunxu HaiEmail author


Insulin resistance (IR) is the hallmark of type 2 diabetes mellitus (T2DM), which is one of the most important chronic noncommunicable diseases. Effective and feasible strategies to treat IR are still urgently needed. Previous research studies reported that whole body vibration (WBV) was beneficial for IR in clinical; however, its underlying mechanisms remains unknown. In the present study, db/db mice were treated with WBV administration 60 min/day for 12 weeks and the impaired insulin sensitivity was improved. Besides, liver steatosis was also ameliorated. Further explorations revealed that WBV could reduce the expression of SREBP1c and increase the expression of GSH-Px and consequently suppress oxidative stress. In conclusion, WBV attenuates oxidative stress to ameliorate liver steatosis and thus improves insulin resistance in db/db mice. Therefore, WBV administration is a promising treatment for individuals who suffered from central obesity and IR.


Insulin resistance Liver steatosis Oxidative stress Glutathione peroxidases Whole body vibration 



This work was supported by Program for Chankiang Scholars, Innovative Research Team in University (PCSIRT) and National Nature Scientific Foundation (NSFC-81473010 and NSFC-3140040159). This work was also supported by the Natural Science Foundation of Shaanxi Province (2014JQ4135).


  1. 1.
    Wild, S., et al. (2004). Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care, 27(5), 1047–1053.CrossRefGoogle Scholar
  2. 2.
    Chan, J. M., et al. (1994). Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care, 17(9), 961–969.CrossRefGoogle Scholar
  3. 3.
    Colditz, G. A., et al. (1995). Weight gain as a risk factor for clinical diabetes mellitus in women. Annals of Internal Medicine, 122(7), 481–486.CrossRefGoogle Scholar
  4. 4.
    Almdal, T., et al. (2004). The independent effect of type 2 diabetes mellitus on ischemic heart disease, stroke, and death: a population-based study of 13,000 men and women with 20 years of follow-up. Archives of Internal Medicine, 164(13), 1422–1426.CrossRefGoogle Scholar
  5. 5.
    Alberti, K. G., & Zimmet, P. Z. (1998). Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabetic Medicine, 15(7), 539–553.CrossRefGoogle Scholar
  6. 6.
    Kahler, W., et al. (1993). Diabetes mellitus--a free radical-associated disease. Results of adjuvant antioxidant supplementation. Zeitschrift fur die Gesamte Innere Medizin und Ihre Grenzgebiete, 48(5), 223–232.Google Scholar
  7. 7.
    Robertson, R., et al. (2007). Chronic oxidative stress as a mechanism for glucose toxicity of the beta cell in type 2 diabetes. Cell Biochemistry and Biophysics, 48(2–3), 139–146.CrossRefGoogle Scholar
  8. 8.
    Choudhury, S., et al. (2015). Inflammation-induced ROS generation causes pancreatic cell death through modulation of Nrf2-NF-kappaB and SAPK/JNK pathway. Free Radical Research 1–41.Google Scholar
  9. 9.
    Kopprasch, S., et al. (2015). Association between systemic oxidative stress and insulin resistance/sensitivity indices - the PREDIAS study. Clinical Endocrinology (Oxf).Google Scholar
  10. 10.
    Pischon, T., et al. (2008). General and abdominal adiposity and risk of death in Europe. The New England Journal of Medicine, 359(20), 2105–2120.CrossRefGoogle Scholar
  11. 11.
    Hassan, H. A., & El-Gharib, N. E. (2015). Obesity and clinical riskiness relationship: therapeutic management by dietary antioxidant supplementation--a review. Applied Biochemistry and Biotechnology, 176(3), 647–669.CrossRefGoogle Scholar
  12. 12.
    Weinheimer-Haus, E. M., et al. (2014). Low-intensity vibration improves angiogenesis and wound healing in diabetic mice. PLoS One, 9(3), e91355.CrossRefGoogle Scholar
  13. 13.
    Kordi Yoosefinejad, A., et al. (2014). The effectiveness of a single session of Whole-Body Vibration in improving the balance and the strength in type 2 diabetic patients with mild to moderate degree of peripheral neuropathy: a pilot study. Journal of Bodywork and Movement Therapies, 18(1), 82–86.CrossRefGoogle Scholar
  14. 14.
    del Pozo-Cruz, B., et al. (2014). Effects of a 12-wk whole-body vibration based intervention to improve type 2 diabetes. Maturitas, 77(1), 52–58.CrossRefGoogle Scholar
  15. 15.
    Rittweger, J. (2010). Vibration as an exercise modality: how it may work, and what its potential might be. European Journal of Applied Physiology, 108(5), 877–904.CrossRefGoogle Scholar
  16. 16.
    Sa-Caputo Dda, C., et al. (2014). Whole body vibration exercises and the improvement of the flexibility in patient with metabolic syndrome. Rehabilitation Research and Practice, 2014, 628518.Google Scholar
  17. 17.
    Bellia, A., et al. (2014). Effects of whole body vibration plus diet on insulin-resistance in middle-aged obese subjects. International Journal of Sports Medicine, 35(6), 511–516.Google Scholar
  18. 18.
    Behboudi, L., et al. (2011). Effects of aerobic exercise and whole body vibration on glycaemia control in type 2 diabetic males. Asian Journal of Sports Medicine, 2(2), 83–90.CrossRefGoogle Scholar
  19. 19.
    Kessler, N. J., & Hong, J. (2013). Whole body vibration therapy for painful diabetic peripheral neuropathy: a pilot study. Journal of Bodywork and Movement Therapies, 17(4), 518–522.CrossRefGoogle Scholar
  20. 20.
    Belavy, D. L., et al. (2014). Preferential deposition of visceral adipose tissue occurs due to physical inactivity. International Journal of Obesity, 38(11), 1478–1480.CrossRefGoogle Scholar
  21. 21.
    Sanudo, B., et al. (2013). Whole body vibration training improves leg blood flow and adiposity in patients with type 2 diabetes mellitus. European Journal of Applied Physiology, 113(9), 2245–2252.CrossRefGoogle Scholar
  22. 22.
    Sun, X., et al. (2012). Activation of peroxisome proliferator-activated receptor-gamma by rosiglitazone improves lipid homeostasis at the adipose tissue-liver axis in ethanol-fed mice. American Journal of Physiology. Gastrointestinal and Liver Physiology, 302(5), G548–G557.CrossRefGoogle Scholar
  23. 23.
    Tan, Y., et al. (2011). Chinese herbal extracts (SK0506) as a potential candidate for the therapy of the metabolic syndrome. Clinical Science (London), 120(7), 297–305.CrossRefGoogle Scholar
  24. 24.
    Arciero, P. J., et al. (2014). Timed-daily ingestion of whey protein and exercise training reduces visceral adipose tissue mass and improves insulin resistance: the PRISE study. J Appl Physiol (1985), 117(1), 1–10.CrossRefGoogle Scholar
  25. 25.
    Kim, H., et al. (2010). (−) Epigallocatechin gallate suppresses the differentiation of 3T3-L1 preadipocytes through transcription factors FoxO1 and SREBP1c. Cytotechnology, 62(3), 245–255.CrossRefGoogle Scholar
  26. 26.
    Lu, C., et al. (2015). Curcumin attenuates ethanol-induced hepatic steatosis through modulating Nrf2/FXR signaling in hepatocytes. IUBMB Life.Google Scholar
  27. 27.
    Feng, R. B., et al. (2015). Crude triterpenoid saponins from Ilex latifolia (Da Ye Dong Qing) ameliorate lipid accumulation by inhibiting SREBP expression via activation of AMPK in a non-alcoholic fatty liver disease model. Chinese Medicine, 10, 23.CrossRefGoogle Scholar
  28. 28.
    Tsedensodnom, O., & Sadler, K. C. (2013). ROS: redux and paradox in fatty liver disease. Hepatology, 58(4), 1210–1212.CrossRefGoogle Scholar
  29. 29.
    Subhapradha, N., et al. (2014). Hepatoprotective effect of beta-chitosan from gladius of Sepioteuthis lessoniana against carbon tetrachloride-induced oxidative stress in Wistar rats. Applied Biochemistry and Biotechnology, 172(1), 9–20.CrossRefGoogle Scholar
  30. 30.
    Liu, W., et al. (2015). Antioxidant mechanisms in nonalcoholic fatty liver disease. Current Drug Targets.Google Scholar
  31. 31.
    Sekiya, M., et al. (2008). Oxidative stress induced lipid accumulation via SREBP1c activation in HepG2 cells. Biochemical and Biophysical Research Communications, 375(4), 602–607.CrossRefGoogle Scholar
  32. 32.
    Chen, Y., et al. (2013). Glutathione defense mechanism in liver injury: insights from animal models. Food and Chemical Toxicology, 60, 38–44.CrossRefGoogle Scholar
  33. 33.
    Meister, A. (1991). Glutathione deficiency produced by inhibition of its synthesis, and its reversal; applications in research and therapy. Pharmacology & Therapeutics, 51(2), 155–194.CrossRefGoogle Scholar
  34. 34.
    Banerjee, M., & Vats, P. (2013). Reactive metabolites and antioxidant gene polymorphisms in Type 2 diabetes mellitus. Redox Biology, 2C, 170–177.Google Scholar
  35. 35.
    Arthur, J. R. (2000). The glutathione peroxidases. Cellular and Molecular Life Sciences, 57(13–14), 1825–1835.Google Scholar
  36. 36.
    Ursini, F., et al. (1995). Diversity of glutathione peroxidases. Methods in Enzymology, 252, 38–53.CrossRefGoogle Scholar
  37. 37.
    Kumar, A. K., & Vijayalakshmi, K. (2015). Protective effect of Punica granatum peel and Vitis vinifera seeds on DEN-induced oxidative stress and hepatocellular damage in rats. Applied Biochemistry and Biotechnology, 175(1), 410–420.CrossRefGoogle Scholar
  38. 38.
    Wang, X., et al. (2015). Association between the NF-E2 related factor 2 gene polymorphism and oxidative stress, anti-oxidative status, and newly-diagnosed type 2 diabetes mellitus in a Chinese population. International Journal of Molecular Sciences, 16(7), 16483–16496.CrossRefGoogle Scholar
  39. 39.
    Forgione, M. A., et al. (2002). Cellular glutathione peroxidase deficiency and endothelial dysfunction. American Journal of Physiology. Heart and Circulatory Physiology, 282(4), H1255–H1261.CrossRefGoogle Scholar
  40. 40.
    Prabhakar, R., Morokuma, K., & Musaev, D. G. (2006). Peroxynitrite reductase activity of selenoprotein glutathione peroxidase: a computational study. Biochemistry, 45(22), 6967–6977.CrossRefGoogle Scholar
  41. 41.
    Demirtas, C. Y., et al. (2015). The investigation of melatonin effect on liver antioxidant and oxidant levels in fructose-mediated metabolic syndrome model. European Review for Medical and Pharmacological Sciences, 19(10), 1915–1921.Google Scholar
  42. 42.
    Guo, R., et al. (2015). Beneficial mechanisms of aerobic exercise on hepatic lipid metabolism in non-alcoholic fatty liver disease. Hepatobiliary & Pancreatic Diseases International, 14(2), 139–144.CrossRefGoogle Scholar
  43. 43.
    Murase, T., et al. (2005). Green tea extract improves endurance capacity and increases muscle lipid oxidation in mice. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 288(3), R708–R715.CrossRefGoogle Scholar
  44. 44.
    Johnson, N. A., Keating, S. E., & George, J. (2012). Exercise and the liver: implications for therapy in fatty liver disorders. Seminars in Liver Disease, 32(1), 65–79.CrossRefGoogle Scholar
  45. 45.
    Cintra, D. E., et al. (2012). Reversion of hepatic steatosis by exercise training in obese mice: the role of sterol regulatory element-binding protein-1c. Life Sciences, 91(11–12), 395–401.CrossRefGoogle Scholar
  46. 46.
    Salminen, A., & Vihko, V. (1983). Lipid peroxidation in exercise myopathy. Experimental and Molecular Pathology, 38(3), 380–388.CrossRefGoogle Scholar
  47. 47.
    Marosi, K., et al. (2012). Long-term exercise treatment reduces oxidative stress in the hippocampus of aging rats. Neuroscience, 226, 21–28.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • Ying Liu
    • 1
  • Mingming Zhai
    • 2
  • Fan Guo
    • 3
  • Tengrui Shi
    • 1
  • Jiangzheng Liu
    • 1
  • Xin Wang
    • 1
  • Xiaodi Zhang
    • 1
  • Da Jing
    • 2
    Email author
  • Chunxu Hai
    • 1
    Email author
  1. 1.Department of Toxicology, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, Shanxi Provincial Key Lab of Free Radical Biology and Medicine, School of Public HealthThe Fourth Military Medical UniversityXi’anPeople’s Republic of China
  2. 2.Department of Biomedical EngineeringThe Fourth Military Medical UniversityXi’anPeople’s Republic of China
  3. 3.Department of Radiology, Xijing HospitalThe Fourth Military Medical UniversityXi’anPeople’s Republic of China

Personalised recommendations