Endocrine

, Volume 29, Issue 1, pp 169–173

Chronic effects of different non-esterified fatty acids on pancreatic islets of rats

Original Articles

Abstract

Aims: The aim of this study was to examine the chronic effects of different non-esterified fatty acids (NEFA) on insulin secretion by pancreatic islets of normal Wistar rats in vitro. Methods: Pancreatic islets were isolated from normal Wistar rats, and were incubated with 0.2, 0.4, or 0.8 mmol/L palmitate (C16:0), stearate (C18:0), oleate (C18:1), or linoleate (C18:2) for 24 h, then the insulin secretion and pyruvate dehydrogenase (PHD) activity were examined. Results: Neither islet insulin content nor islet DNA content differed among islets incubated with each kind of NEFA. Compared with control, linoleate significantly inhibited glucose-stimulated insulin secretion (GSIS) and PDH activity at each concentration (p<0.05), while others inhibited GSIS and PDH activity significantly only at 0.4 and 0.8 mmol/L (p<0.05). There was no significant difference in GSIS and PDH activity among islets pretreated by palmitate, stearate, and oleate at the same concentration (p>0.05). However, linoleate decreased GSIS more than others at the same concentration (p<0.05), while linoleate (0.4 or 0.8 mmol/L) inhibited PDH activity more than others at the same concentration (p<0.05). Conclusions: Elevation of palmitate, stearate, oleate or linoleate decreases the β-cell secretory response to glucose, through inhibiting PDH activity. Linoleate exerts more negative effect on GSIS than other NEFA.

Key Words

Non-esterified fatty acids pancreatic islet insulin secretion glucose intolerance pyruvate dehydrogenase 

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References

  1. 1.
    King, H., Aubert, R. E., and Herman, W. H. (1998). Diabetes Care 21, 1414–1431.PubMedCrossRefGoogle Scholar
  2. 2.
    Unger, R. (1995). Diabetes 44, 863–870.PubMedCrossRefGoogle Scholar
  3. 3.
    Mason, T. M., Goh, T., Tchipashvili, V., et al. (1999). Diabetes 48, 524–530.PubMedCrossRefGoogle Scholar
  4. 4.
    Zhou, Y. P. and Grill, V. E. (1994). J. Clin. Invest. 93, 870–876.PubMedGoogle Scholar
  5. 5.
    Sako, Y. and Grill, V. E. (1990). Endocrinology 127, 1580–1589.PubMedCrossRefGoogle Scholar
  6. 6.
    Tamarit-Rodriguez, J., Vara, E., and Tamarit, J. (1984). Biochem. J. 221, 317–324.PubMedGoogle Scholar
  7. 7.
    Warnotte, C., Gilon, P., Nenquin, M., and Henquin, J. C. (1994). Diabetes 43, 703–711.PubMedCrossRefGoogle Scholar
  8. 8.
    Conget, I., Rasschaert, J., Sener, A., et al. (1994). Biochem. Med. Metab. Biol. 51, 175–184.PubMedCrossRefGoogle Scholar
  9. 9.
    Opara, E. C., Garfitel, M., Hubbard, V. S., Burch, W. M., and Akwari, O. E. (1994). Am. J. Physiol. 266, E635–639.PubMedGoogle Scholar
  10. 10.
    Stein, D. T., Stevenson, B., Chester, M., et al. (1997). J. Clin. Invest. 100, 398–403.PubMedGoogle Scholar
  11. 11.
    Wang, Y., Miura, Y., Kaneko, T., et al. (2002). Endocrine 17, 185–191.PubMedCrossRefGoogle Scholar
  12. 12.
    Collier, G. R., Chisholm, K., Sykes, S., Dryden, P. A., and O'Dea, K. (1985). J. Nutr. 115, 1471–1476.PubMedGoogle Scholar
  13. 13.
    Tsunoda, N., Ikemono, S., Takahashi, M., et al. (1998). Metabolism 47, 724–730.PubMedCrossRefGoogle Scholar
  14. 14.
    Akiyama, T., Tachibana, I., Shirohara, H., Watanabe, N., and Otsuki, M. (1996). Diabetes Res. Clin. Pract. 31, 27–35.PubMedCrossRefGoogle Scholar
  15. 15.
    Wang, Y., Wang, P. Y., Qin, L. Q., et al. (2003). Endocrine 22, 85–92.PubMedCrossRefGoogle Scholar
  16. 16.
    Randle, P. J. (1993). Diabetologia 36 269–275.PubMedCrossRefGoogle Scholar
  17. 17.
    Randle, P. J. (1995). Proc. Nutr. Soc. 54, 317–327.PubMedCrossRefGoogle Scholar
  18. 18.
    Randle, P. J., Priestman, D. A., Mistry, S. C., and Halsball, A. (1994). J. Cell Biochem. 55 S 1–11.PubMedCrossRefGoogle Scholar
  19. 19.
    Hu, F. B., van Dam, R. M., and Liu, S. (2001). Diabetologia 44, 805–817.PubMedCrossRefGoogle Scholar
  20. 20.
    Vessby, B., Aro, A., Skarfors, E., Berglund, L., Salminen, I., and Lithell, H. (1994). Diabetes 43, 1353–1357.PubMedCrossRefGoogle Scholar
  21. 21.
    Vessby, B., Uusitupa, M., Hermansen, K., et al. (2001). Diabetologia 44, 312–319.PubMedCrossRefGoogle Scholar
  22. 22.
    Warnotte, C., Nenquin, M., and Henquin, J. C. (1999). Mol. Cell. Endocrinol. 153, 147–153.PubMedCrossRefGoogle Scholar
  23. 23.
    Zhou, Y. P. and Grill, V. E. (1995). Diabetes 44, 394–399.PubMedCrossRefGoogle Scholar
  24. 24.
    Lupi, R. and Dotta, F. (2002). Diabetes 51, 1437–1442.PubMedCrossRefGoogle Scholar
  25. 25.
    Lameloise, N., Muzzin, P., Marc, P., and Assimacopoulos-Jeannet, F. (2001). Diabetes 50, 803–809.PubMedCrossRefGoogle Scholar
  26. 26.
    Miura, Y. and Matsui, H. (2001). Toxicol. Appl. Pharmacol. 174, 1–9.PubMedCrossRefGoogle Scholar
  27. 27.
    Ishihara, F., Aizawa, T., Taguchi, N., Sato, Y., and Hashizume, K. (1994). J. Endocrinol. 143, 497–503.PubMedGoogle Scholar
  28. 28.
    Labarca, C. and Paigen, K. (1980). Anal. Biochem. 102, 344–352.PubMedCrossRefGoogle Scholar
  29. 29.
    Hopcroft, D. W., Mason, D. R., and Scott, R. S. (1985). Horm. Metab. Res. 17, 559–561.PubMedGoogle Scholar
  30. 30.
    Paxton, R., Harris, A., Sener, A., and Malaisse, W. J. (1988). Horm. Metab. Res. 20, 317–322.PubMedCrossRefGoogle Scholar
  31. 31.
    Goodwin, G. W., Zhang, B., Paxton, R., and Harris, R. A. (1988). Methods Enzymol. 166, 189–201.PubMedCrossRefGoogle Scholar

Copyright information

© Humana Press Inc. 2006

Authors and Affiliations

  1. 1.Department of Endocrinology, The 4th Affiliated HospitalHeBei Medical UniversityShiJiazhuang, HeBeiChina
  2. 2.Department of Health Sciences, Medical SchoolPeking UniversityPekingChina
  3. 3.Yamanashi Health HospitalYamanashiJapan

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