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Neuroscience and Behavioral Physiology

, Volume 37, Issue 4, pp 341–347 | Cite as

Transcranial electrostimulation activates reparative regeneration and the insulin-producing function of pancreatic B-cells in alloxan diabetes in rats

  • V. P. Lebedev
  • S. V. Bilichenko
  • N. É. Ordyan
  • S. G. Pivina
  • S. P. Nechiporenko
  • A. A. Puzyrev
  • E. A. Mikheeva
  • K. K. Kubacheva
Article
  • 59 Downloads

Abstract

Studies on rats with experimental diabetes induced by administration of alloxan showed that transcranial electrostimulation of endorphinergic brain structures stimulates the regeneration of damaged β-cells in pancreatic islets of Langerhans. This was identified on pancreatic sections stained with hematoxylin and eosin. De novo formation of small islets was noted, as evidenced by their regeneration from progenitor cells. After transcranial electrostimulation, islet β-cells stained by the Gomori method showed recovery of granularity-a sign of insulin production. Application of an immunoenzyme method demonstrated recovery of blood insulin levels, the dynamics of increases in which showed a highly significant negative correlation with a decrease in blood glucose. These data led to the conclusion that the antihyperglycemic effect of transcranial electrostimulation in experimental alloxan diabetes results from reparative regeneration of β-cells in islets of Langerhans with recovery of their insulin-producing function.

Key words

alloxan diabetes transcranial electrostimulation antihyperglycemic effect islet of Langerhans β-cells reparative regeneration insulin production 

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References

  1. 1.
    L. N. Airapetyants, A. M. Zaichik, M. S. Trukhmanov, V. P. Lebedev, et al., “Changes in β-endorphin levels in the brain and cerebrospinal fluid during transcranial electroanalgesia,” Ros. Fiziol. Zh. im. I. M. Sechenova, 71 No. 1, 56–63, (19Google Scholar
  2. 2.
    V. A. Aleksandrova, S. V. Rychkova, V. P. Lebedev, et al., “Effects of transcranial electrostimulation of brain opioid structures on the regeneration of ulcers in the gastric mucosa and duodenal,” Mezhdunarod. Med. Obzory, 1, 41–46 (1994).Google Scholar
  3. 3.
    G. N. Alieva, A. P. Kiyasov, M. M. Minnebaev, I. M. Burykin, and R. Kh. Khafiz’yanova, “Dynamics of pancreatic β-and α-cell populations and blood glucose levels in alloxan diabetes,” Byull. Éksperim. Biol. Med., 133, No. 2, 141–153 (2002).CrossRefGoogle Scholar
  4. 4.
    V. G. Baranov, N. M. Sokoloverova, É. G. Gasparyan, and Yu.A. Yaroshevskii, Experimental Diabetes Mellitus [in Russian], Nauka, Leningrad (1983).Google Scholar
  5. 5.
    Kh. Kh. Dorshe and S. von Falkmer, “Ontogenesis of human islets of Langerhans. A review of light and electron microscope, immunohistochemical, and functional data on fetal development of the endocrine pancreas,” Zh. Évolyuts. Biokhim. Fiziol., 36, No. 6, 527–552 (2000).Google Scholar
  6. 6.
    B. A. Kudryashev and A. M. Ul’yanov, “Stable decreases in insulin production in experimental insulin-dependent diabetes,” Vopr. Med. Khimii, 37, No. 4, 40–43 (1991).Google Scholar
  7. 7.
    V. P. Lebedev, S. V. Bilichenko, A. V. Malygin, S. P. Nechiporenko, S. E. Kabasov, and M. V. Melikhova, “Transcranial electrostimulation normalizes blood sugar levels in alloxan diabetes in rats,” Ros. Fiziol. Zh. im. I. M. Sechenova, 90, No. 11, 1426–1429 (2004).Google Scholar
  8. 8.
    V. P. Lebedev, M. V. Melikhova, S. E. Kolbasov, G. S. Stroikova, and O. N. Zamuruev, “Effects of transcranial electrostimulation of endorphin brain structures in rats on the functional activity of hepatocytes subject to toxic damage,” Ros. Fiziol. Zh. im. I. M. Sechenova, 86, No. 11, 1449–1557 (2000).Google Scholar
  9. 9.
    A. A. Puzyrev, “Formation of human pancreatic endocrine cells from the epithelium of ducts and acini,” Arkh. Anat. Gistol. Émbriol., 76, No. 1, 20–25 (1979).PubMedGoogle Scholar
  10. 10.
    A. A. Puzyrev, “Differentiation of pancreatic endocrine cells in white rats within the epithelium of output ducts,” Arkh. Anat. Gistol. Émbriol., 82, No. 3, 83–90 (1982).PubMedGoogle Scholar
  11. 11.
    É. S. Severgina, T. G. Dyuzheva, L. E. Razgulina, and I. B. Stakheev, “Location of β-cells in acini-normal appearances or signs of a compensatory process in insulin-dependent diabetes mellitus,” Arkh. Patol., 52, No. 12, 18–23 (1992).Google Scholar
  12. 12.
    N. U. Tits, Encyclopedia of Clinical and Laboratory Tests [in Russian], Labinform, Moscow (1997).Google Scholar
  13. 13.
    P. L. Brukbaker, A. Sun, and M. Vranic, “Lack of effect of beta-endorphin on basal or glucagon-stimulated hepatic glucose production in vitro,” Metabolism, 36, No. 5, 432–437 (1987).CrossRefGoogle Scholar
  14. 14.
    C. Y. Cheynga and F. Tang, “On effect of streptozotocin-diabetes on beta-endorphin level and proopiomelanocortin gene expression in the rat pituitary,” Neurosci. Lett., 26, No. 1–2, 118–120 (1999).CrossRefGoogle Scholar
  15. 15.
    D. L. Eizirik, D. G. Pipeleers, Z. Ling, N. Welsh, et al., “Major species differences between humans and rodents in the susceptibility to pancreatic beta-cell injury,” Proc. Natl. Acad. Sci. USA, 91, No. 20, 9253–9256 (1994).PubMedCrossRefGoogle Scholar
  16. 16.
    M. Elsner, M. Tiedge, B. Guldbakke, R. Munday, and S. Lenzen, “Importance of the GLUT2 glucose transporter for pancreatic beta cell toxicity of alloxan,” Diabetologia, 45, No. 11, 1542–1549 (2002).PubMedCrossRefGoogle Scholar
  17. 17.
    A. A. Evans, S. Khan, and M. E. Smith, “Evidence for a hormonal action of beta-endorphin to increase glucose uptake in resting and contracting skeletal muscle,” J. Endocrinol., 155, No. 2, 387–392 (1997).PubMedCrossRefGoogle Scholar
  18. 18.
    I. G. Fatouros, A. H. Goldfarb, A. Z. Jamurtas, T. J. Angelopoulos, and J. Gao, “Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats,” Eur. J. Appl. Physiol. Occup. Physiol., 76, No. 3, 203–208 (1997).PubMedCrossRefGoogle Scholar
  19. 19.
    H. Gunoz, A. Dindar, and O. Neyzi, “Beta-endorphin and some hormonal levels in children with acute stress hyperglycaemia,” Diabetes Res. Clin. Pract., 24, No. 2, 97–101 (1994).PubMedCrossRefGoogle Scholar
  20. 20.
    Y. Izumida, T. Aoki, D. Yasuda, T. Koizumi, C. Suganuma, et al., “Hepatocyte growth factor is constitutively produced by donor-derived bone marrow cells and promotes regeneration of pancreatic beta-cells,” Biochem. Biophys. Res. Commun., 333, No. 1, 273–282 (2005).PubMedCrossRefGoogle Scholar
  21. 21.
    J. Kamei, “Antinociceptive effects of the enantiomorphs and its main metabolite in streptozotocin-induced diabetic mice,” Nihon Shinkei Seishin Yakurigaku Zasshi., 20, No. 1, 11–16 (2000).PubMedGoogle Scholar
  22. 22.
    D. Kirpicnikov, S. I. McFarlane, and J. R. Sowers, “Metformin: an update,” Ann. Intern. Med., 137, No. 1, 25–33 (2002).Google Scholar
  23. 23.
    I. M. Liu, C. S. Niu, T. C. Chi, D. H. Kuo, and J. T. Cheng, “Investigations of the mechanism of the reduction of plasma glucose by cold-stress in streptozotocin-induced diabetic rats,” Neurosci., 92, No. 3, 1137–1142 (1999).CrossRefGoogle Scholar
  24. 24.
    M. Matsumura, T. Fukushima, H. Saito, and S. Saito, “In vivo and in vitro effects of beta-endorphin on glucose metabolism in the rat,” Horm. Metabolism. Res., 16, No. 1, 27–31 (1984).CrossRefGoogle Scholar
  25. 25.
    N. Passariello, G. Giugliano, A. Quatraro, G. Consoli, S. Sgambato, R. Torella, and F. D’Onofrio, “ Glucose tolerance and hormonal responses in heroin addicts. A possible role for endogenous opiates in the pathogenesis on of non-insulin-diabetes dependent,” Metabolism, 32, No. 12, 1163–1165 (1983).PubMedCrossRefGoogle Scholar
  26. 26.
    J. M. Slack, “Developmental biology of pancreas,” Development, 121, No. 6, 1569–1580 (1995).PubMedGoogle Scholar
  27. 27.
    M. Waguri, K. Yamamoto, J. Y. Miygawa, Y. Tochino, K. Yamamori, et al., “Demonstration of two different processes of beta-cell regeneration in a new diabetic mouse model induced by selective perfusion of alloxan,” Diabetes, 46, No. 8, 1281–1290 (1997).PubMedCrossRefGoogle Scholar
  28. 28.
    S. S. Walde, C. Dohle, P. Schott-Ohly, and H. Gleichmann, “Molecular target structures in alloxan-induced diabetes in mice,” Life Sci., 81, No. 14, 1681–1694 (2002).CrossRefGoogle Scholar
  29. 29.
    R. Wang, N. Yashpal, F. Bacchus, and J. J. Li, “Hepatocyte growth factor regulates proliferation and differentiation of epithelial monolayers derived from islets of postnatal rat pancreas,” Endocrinol., 183, No. 1, 163–171 (2004).CrossRefGoogle Scholar
  30. 30.
    M. Zhang, M. Zheng, and R. L. Schleicher, “Autoradiographic localization of beta-endorphin binding in the pancreas,” Mol. Cell Neurosci., 5, No. 6, 684–690 (1994).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2007

Authors and Affiliations

  • V. P. Lebedev
    • 1
  • S. V. Bilichenko
    • 1
    • 2
  • N. É. Ordyan
    • 1
  • S. G. Pivina
    • 1
  • S. P. Nechiporenko
    • 2
  • A. A. Puzyrev
    • 3
  • E. A. Mikheeva
    • 3
  • K. K. Kubacheva
    • 4
  1. 1.I. P. Pavlov Institute of PhysiologyRussian Academy of SciencesSt. PetersburgRussia
  2. 2.Institute of ToxicologyMinistry of Health of the Russian FederationSt. PetersburgRussia
  3. 3.I. I. Mechnikov State Medical AcademySt. PetersburgRussia
  4. 4.Postgraduate Medical AcademySt. PetersburgRussia

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