Bulletin of Experimental Biology and Medicine

, Volume 156, Issue 5, pp 649–653 | Cite as

Rats of Hypertensive ISIAH Strain are Resistant to the Development of Metabolic Syndrome Induced by High-Fat Diet

  • M. I. Dushkin
  • M. V. Khrapova
  • G. G. Kovshik
  • M. I. Chasovskikh
  • V. G. Selyatitskaya
  • N. A. Palchikova
Article
  • 67 Downloads

We studied the influence of high-fat diet on the development of metabolic syndrome in rats of hypertensive ISIAH strain and normotensive WAG strain. In contrast to ISIAH rats, highfat diet in WAG rats led visceral obesity, glucose tolerance, and dyslipidemia. DNA-binding activity of the peroxisome proliferator-activated receptor α (PPARα) decreased in the liver of WAG rats and increased in ISIAH rats. Blood levels of TNF-α, IL-6, and corticosterone increased more significantly in WAG rats. Corticosterone content in the adrenal glands was more markedly reduced in WAG rats. High-fat diet had no effect on BP in ISIAH and WAG rats. It was concluded that ISIAH rats can be used as a genetic model in studies of the mechanism of resistance to the metabolic syndrome.

Key Words

hypertensive ISIAH rat strain high-fat diet resistance to metabolic syndrome 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    M. I. Dushkin and M. V. Khrapova, Uspekhi Fiziol. Nauk, 42, No. 2, 3-24 (2011).Google Scholar
  2. 2.
    E. L. Gibson, Physiol. Behav., 89, No. 1, 53-61 (2006).PubMedCrossRefGoogle Scholar
  3. 3.
    J. Han, D. M. Jiang, C. Q. Du, and S. J. Hu, Circ. J., 75, No. 6, 1409-1417 (2011).PubMedCrossRefGoogle Scholar
  4. 4.
    A. Hattori, K. Mawatari, S. Tsuzuki, et al., Obesity (Silver Spring), 18, No. 1, 48-54 (2010).CrossRefGoogle Scholar
  5. 5.
    J. M. Helies, A. Diane, A. Langlois, et al., Obes. Res., 13, No. 1, 3-10 (2005).PubMedCrossRefGoogle Scholar
  6. 6.
    S. Hojna, M. D. Jordan, H. Kollias, and Z. Pausova, Hypertens. Res., 35, No. 3, 279-286 (2012).PubMedCrossRefGoogle Scholar
  7. 7.
    D. D. Kitts, Y. V. Yuan, and D. V. Godin, Can. J. Physiol. Pharmacol., 76, No. 2, 202-209 (1998).PubMedCrossRefGoogle Scholar
  8. 8.
    L. Malerod, L. K. Juvet, A. Hanssen-Bauer, et al., Biochem. Biophys. Res. Commun., 299, No. 5, 916-923 (2002).PubMedCrossRefGoogle Scholar
  9. 9.
    N. Marissal-Arvy, A. Gaumont, A. Langlois, et al., J. Endocrinol., 195, No. 3, 473-484 (2007).PubMedCrossRefGoogle Scholar
  10. 10.
    N. Marissal-Arvy, A. Langlois, C. Tridon, and P. Mormede, Metabolism, 60, No. 5, 706-719 (2011).PubMedCrossRefGoogle Scholar
  11. 11.
    A. L. Markel, O. E. Redina, M. A. Gilinsky, et al., J. Endocrinol.,195, No. 3, 439-450 (2007).PubMedCrossRefGoogle Scholar
  12. 12.
    D. Perrin, J. Mamet, A. Geloen, et al., Auton Neurosci., 109, Nos. 1-2, 1-9 (2003).PubMedCrossRefGoogle Scholar
  13. 13.
    A. C. Shin, S. M. MohanKumar, M. P. Sirivelu, et al., Int. J. Obes. (Lond.), 34, No. 7, 1218-1226 (2010).CrossRefGoogle Scholar
  14. 14.
    J. Van den Brandt, P. Kovacs, and I. Kloting, Int. J. Obes. Relat. Matab. Disord., 24, No. 12, 1618-1622 (2000).CrossRefGoogle Scholar
  15. 15.
    X. Wang, A. Ge, M. Cheng, et al., Exp. Diabetes Res., 2012, doi: 10.1155/2012/847246 (2012).

Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • M. I. Dushkin
    • 1
    • 2
  • M. V. Khrapova
    • 1
    • 2
  • G. G. Kovshik
    • 1
  • M. I. Chasovskikh
    • 1
  • V. G. Selyatitskaya
    • 3
  • N. A. Palchikova
    • 3
  1. 1.Research Institute of PhysiologySiberian Division of the Russian Academy of Medical SciencesNovosibirskRussia
  2. 2.Research Institute of TherapySiberian Division of the Russian Academy of Medical SciencesNovosibirskRussia
  3. 3.Research Center of Clinical and Experimental MedicineSiberian Division of the Russian Academy of Medical SciencesNovosibirskRussia

Personalised recommendations