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Neuroscience and Behavioral Physiology

, Volume 28, Issue 1, pp 1–7 | Cite as

Neuroendocrine control of the gonadotropic function of the hypophysis in experimental diabetes

  • V. N. Babichev
  • E. I. Adamskaya
  • T. A. Kuznetsova
  • I. V. Shishkina
Article

Conclusions

  1. 1.

    Development of experimental diabetes in male rats is associated with reductions in the blood T concentration and in the number of nuclear androgen receptors in the adenohydraphysis. Blood LH and FSH levels did not change.

     
  2. 2.

    The LH-RH sensitivity of the hypophysis in STZ-treated male rats decreased sharply on incubation for more than 1h.

     
  3. 3.

    Administration of STZ to female rats led to disruption of the estral cycle, accompanied by a reductions in the cyclic secretion of gonadotropins and sex hormones.

     
  4. 4.

    The development of diabetes in cycling female rats led to a reduction in the concentration of nuclear E2 receptors in the PR and hypophysis, and the number of T-binding sites decreased only in the hypophysis.

     
  5. 5.

    The gonadotropin wave stimulated by sex steroids in ovariectomized female rats with diabetes was significantly reduced, due to changes in the activity of the LH-RH-producing system.

     

Keywords

Luteinizing Hormone Medial Eminence Experimental Diabetes Luteinizing Hormone Secretion Luteinizing Hormone Concentration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    V. N. Babichev, E. I. Adamskaya, and V. M. Samosonova, Probl. Éndokrinol., No. 4, 63–68 (1975).Google Scholar
  2. 2.
    V. N. Babichev, T. A. Peryshkova, and L. Yu. Ozol', Probl. Éndokrinol., No. 6, 46–51 (1983).Google Scholar
  3. 3.
    V. N. Babichev, T. A. Peryshkova, and E. I. Adamskaya, Probl. Éndokrinol., No. 2, 59–62 (1989).Google Scholar
  4. 4.
    V. N. Babichev, T. A. Peryshkova, and E. I. Adamskaya, Probl. Éndokrinol., No. 1, 42–45 (1993).Google Scholar
  5. 5.
    V. N. Babichev, T. A. Peryshkova, and E. I. Adamskaya, Probl. Éndokrinol., No. 1, 43–46 (1994).Google Scholar
  6. 6.
    T. A. Peryshkova and V. N. Babichev, Probl. Éndokrinol., No. 6, 41–44 (1989).Google Scholar
  7. 7.
    G. Bestetti, V. Locatelli, F. Tirone, et al., Endocrinology,117, 208–216 (1985).PubMedGoogle Scholar
  8. 8.
    F. Homo-Delarche, F. Fitzpatrick, and N. Christeff, J. Steroid Biochem.,40, 619–637 (1991).CrossRefGoogle Scholar
  9. 9.
    S. Katayama, C. M. Brownsheidle, V. Wootten, et al., Diabetes,33, 324–327 (1984).PubMedGoogle Scholar
  10. 10.
    T. S. King, D. N. Rohrbach, A. L. Miller, et al., Biomed. Res.,8, 37–143 (1987).Google Scholar
  11. 11.
    T. S. King and I. S. Kang, Biochem. Res.,10, 333–339 (1989).Google Scholar
  12. 12.
    T. S. King and D. N. Rohrback, Exp. Brain Res.,81, 619–625 (1990).PubMedCrossRefGoogle Scholar
  13. 13.
    A. Sahu, C. A. Sninsky, and P. S. Kalra, Endocrinology,126, 192–198 (1990).PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Publishing Corporation 1998

Authors and Affiliations

  • V. N. Babichev
  • E. I. Adamskaya
  • T. A. Kuznetsova
  • I. V. Shishkina

There are no affiliations available

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