Skip to main content
SpringerLink
Log in

Serum and gene expression levels of leptin and adiponectin in rats susceptible or resistant to diet-induced obesity

Niveles séricos y expresión de los genes de leptina y adiponectina en ratas susceptibles o resistentes al desarrollo de obesidad inducida por la dieta

  • Published:
Journal of Physiology and Biochemistry Aims and scope Submit manuscript

Abstract

The aim of the present study was to identify the role of leptin and adiponectin in the development of resistance or susceptibility to diet-induced obesity in rats. For this purpose, male Wistar rats were fed with standard laboratory diet (control group) or cafeteria diet. After 15 days, two groups of rats with different response respect to the cafeteria diet were identified, and were assigned as diet-induced obesity (DIO) and diet resistant (DR) rats. The high-fat diet induced a very dignificant increase in both body and fat mass weight in DIO group. However, DR rats, gained even less weight than control-fed animals. Food intake was increased in cafeteria-fed rats (both DIO and DR) in comparison to control group; but hyperphagia was higher in DIO rats. In addition, feed efficiency (the ratio of weight gained to calories consumed) was significantly decreased in DR as compared to DIO rats. Regarding leptin, a significant increase in both adipose tissue gene expression and serum levels was observed in DIO rats in comparison with other groups (control and DR). A significant increase in both adiponectin circulating levels and adipose tissue mRNA expression was also observed in DIO animals as compared with the other groups. These data suggest that the susceptibility to obesity of DIO rats might be secondary, at least in part, to an earlier development of leptin resistance, which could lead to alterations in food intake (hyperphagia) and energetic metabolism. However, neither changes in leptin or adiponectin seem to be involved in the adaptive mechanisms that confer resistance to high fat intake.

Resumen

En el presente trabajo, se estudia el papel de la leptina y la adiponectina en la resistencia o susceptibilidad a la obesidad inducida por la dieta. Para ello, se alimentaron ratas Wistar macho con una dieta de laboratorio (grupo control) o con una dieta rica en grasa (dieta de cafetería). Tras 15 días, se identificaron dos grupos de ratas con diferente respuesta a la dieta de cafetería, los cuales fueron designados como susceptibiles (DIO) o resistentes (DR) al desarrollo de obesidad. Así, se observó un incremento muy significativo en el peso y la masa grasa corporal en el grupo DIO, mientras que los animales del grupo DR ganaron menos peso corporal que los animales control. La ingesta calórica fue significativamente superior en los grupos DR y DIO respecto del grupo control, aunque la hiperfagia fue significativamente superior en los animales susceptibles. Además, la eficiencia metabólica fue significativamente inferior en las ratas DR. En cuanto a la leptina y a la adiponectina, las ratas DIO mostraron un incremento significativo tato en la expresión de los genes correspondientes en tejido adiposo como en los niveles séricos de ambas hormonas. Esto datos sugieren que la susceptibilidad a la obesidad en las ratas DIO podría ser secundaria a un desarrollo temprano de resistencia a la leptina, que puede ir acompañada tanto de alteraciones en la ingesta (hiperfagia) como en el metabolismo energético. Sin embargo, ni los cambios en la leptina ni en la adiponectina parecen estar implicados en los mecanismos de adaptación que provocan resistencia a la obesidad.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Arita, Y., Kihara, S., Ouchi, N., Takahashi, M., Maeda, K., Miyagawa, J., Hotta, K., Shimomura, I., Nakamura, T., Miyaoka, K., Kuriyama, H., Nishida, M., Yamashita, S., Okubo, K., Matsubara, K., Muraguchi, M., Ohmoto, Y., Funahashi, T. and Matsuzawa, Y. (1999):Biochem. Biophys. Res. Commun.,257, 79–83.

    Article  CAS  PubMed  Google Scholar 

  2. Berraondo, B., Marti, A., Duncan, J.S., Trayhurn, P. and Martínez, J. A. (2000):Int. J. Obes. Relat. Metab. Disord.,24, 156–163.

    Article  CAS  PubMed  Google Scholar 

  3. Bullen, J. W., Jr., Ziotopoulou, M., Ungsunan, L., Misra, J., Alevizos, I., Kokkotou, E., Maratos-Flier, E., Stephanopoulos, G. and Mantzoros, CS. (2004):Am. J. Physiol. Endocrinol. Metab.,287, E662–670.

    Article  CAS  PubMed  Google Scholar 

  4. Caro, J. F., Sinha, M. K., Kolaczynski, J. W., Zhang, P. L. and Considine, R. V. (1996):Diabetes,45, 1455–1462.

    CAS  PubMed  Google Scholar 

  5. Chang, S., Graham, B., Yakubu, F., Lin, D., Peters, J. C. and Hill, J.O. (1990):Am. J. Physiol.,259, R1103–1110.

    CAS  PubMed  Google Scholar 

  6. Collins, S., Martin, T. L., Surwit, R. S. and Robidoux, J. (2004):Physiol. Behav.,81, 243–248.

    Article  CAS  PubMed  Google Scholar 

  7. Havel, P. J. (2004):Diabetes,53,Suppl 1, S143-S151.

    Article  CAS  PubMed  Google Scholar 

  8. Hotta, K., Funahashi, T., Bodkin, N. L., Ortmeyer, H. K., Arita, Y. and Hansen, B. C. (2001):Diabetes,50, 1126–1133.

    Article  CAS  PubMed  Google Scholar 

  9. Hu, E., Liang, P. and Spiegelman, B. M. (1996):J. Biol. Chem.,271, 10697–10703.

    Article  CAS  PubMed  Google Scholar 

  10. Ioffe, E., Moon, B., Connolly, E. and Friedman, J. M. (1998):Proc. Natl. Acad. Sci.,95, 11852–11857.

    Article  CAS  PubMed  Google Scholar 

  11. Jang, I., Hwang, D., Lee, J., Chae, K., Kim, Y. and Kang, T. (2003):Exp. Anim.,52, 99–107.

    Article  CAS  PubMed  Google Scholar 

  12. Kubota, N., Terauchi, Y., Yamauchi, T., Kubota, T., Moroi, M., Matsui, J., Eto, K., Yamashita, T., Kamon, J., Satoh, H., Yano, W., Froguel, P., Nagai, R., Kimura, S., Kadowaki, T. and Noda, T. (2002):J. Biol. Chem.,277, 25862–25866.

    Google Scholar 

  13. Levin, B. E. and Keesey, R. E. (1998):Am. J. Physiol.:274, 412–419.

    Google Scholar 

  14. Levin, B. E. (1999):Am. J. Physiol.,276, 382–387.

    Google Scholar 

  15. Levin, B. E. and Dunn-Meynell, A. A. (2000):Am. J. Physiol. Regul. Integr. Comp. Physiol.,278, 231–237.

    Google Scholar 

  16. Levin, B. E. and Dunn-Meynell, A. A. (2002):Am. J. Physiol. Regul. Integr. Comp. Physiol.,282, 46–54

    Google Scholar 

  17. Levin, B. E., Dunn-Meynell, A. A., Ricci, M. R. and Cummings, D. E. (2003):Am. J. Physiol. Endocrinol. Metab.,285, 949–957.

    Google Scholar 

  18. Levin, B. E., Dunn-Meynell, A. A. and Banks, W. A. (2004):Am. J. Physiol. Regul. Integr. Comp. Physiol.,286, 143–150.

    Google Scholar 

  19. Li, J., Yu, X., Pan, W. and Unger, R. H. (2002):Am. J. Physiol. Endocrinol. Metab.,282, E1334–1341.

    CAS  PubMed  Google Scholar 

  20. Loos, R. J. and Bouchard, C. (2003):J. Intern. Med.,254, 401–425.

    Article  CAS  PubMed  Google Scholar 

  21. Lopez, I. P., Milagro, F. I., Marti, A., Moreno-Aliaga, M. J., Martínez, J. A. and De Miguel, C. (2004):Biochem. Biophys. Res. Commun.,318, 234–239.

    Article  CAS  PubMed  Google Scholar 

  22. Maeda, N., Shimomura, I., Kishida, K., Nishizawa, H., Matsuda, M., Nagarentani, H., Furuyama, N., Kondo, H., Takahashi, M., Arita, Y., Komuro, R., Ouchi, N., Kihara, S., Tochino, Y., Okutomi, K., Horie, M., Takeda, S., Aoyama, T., Funahashi, T. and Matsuzawa, Y. (2002):Nat. Med.,8, 731–737.

    Article  CAS  PubMed  Google Scholar 

  23. Maffei, M., Halaas, J., Ravussin, E., Pratley, R. E., Lee, G. H., Zhang, Y., Fei, H., Kim, S., Lallone, R. and Ranganathan, S. (1995):Nat. Med.,1, 1155–1161.

    Article  CAS  PubMed  Google Scholar 

  24. Margareto, J., Marti, A. and Martínez, J. A. (2001):J. Physiol. Biochem.,57, 347–348.

    CAS  PubMed  Google Scholar 

  25. Marti, A., Berraondo, B. and Martínez, J. A. (1999):J. Physiol. Biochem.,55, 43–49.

    CAS  PubMed  Google Scholar 

  26. Meier, U. and Gressner, A. M. (2004):Clin. Chem.,50, 1151–1525.

    Article  CAS  Google Scholar 

  27. Montague, C. T., Farooqi, I. S., Whitehead, J. P., Soos, M. A., Rau, H., Wareham, N. J., Sewter, C. P., Digby, J. E., Mohammed, S. N., Hurst, J. A., Cheetham, C. H., Earley, A. R., Barnett, A. H., Prins, J. B. and O’Rahilly, S. (1997):Nature,387, 903–908.

    Article  CAS  PubMed  Google Scholar 

  28. Moreno, M. J. and Martínez, J. A. (2002):Anales sist. San. Navarra,25,Suppl 1, 29–39.

    Google Scholar 

  29. Moreno-Aliaga, M. J., Lamas, O., Marti, A. and Martínez, J. A. (2002):Biochem. Biophys. Res. Commun.,291, 1201–1207.

    Article  CAS  PubMed  Google Scholar 

  30. Moreno-Aliaga, M. J., Urresti, J., Lamas, O., Marti, A. and Martínez, J. A. (2003):Int. J. Obes.,37 (Supp. 1), S 56.

    Google Scholar 

  31. Morton, N. M., Paterson, J. M., Masuzaki, H., Holmes, M. C., Staels, B., Fievet, C., Walker, B. R., Flier, J. S., Mullins, J. J. and Seckl, J. R. (2004):Diabetes,53, 931–938.

    Article  CAS  PubMed  Google Scholar 

  32. Munzberg, H., Flier, J. S. and Bjorbaek, C. (2004):Endocrinology,145, 4880–4889.

    Article  PubMed  CAS  Google Scholar 

  33. Pérez-Matute, P., Marti, A., Martínez, J. A. and Moreno-Aliaga, M. J. (2003):J. Physiol. Biochem.,59, 201–208.

    Article  PubMed  Google Scholar 

  34. Qi, Y., Takahashi, N., Hileman, S. M., Patel, H. R., Berg, A. H. and Pajvani, U. B., Scherer P. E. and Ahima R. S. (2004):Nat. Med. 10, 524–529

    Article  CAS  PubMed  Google Scholar 

  35. Stefan, N. and Stumvoll, M. (2000):Horm. Metab. Res.,34, 469–474.

    Article  Google Scholar 

  36. Surwit, R. S., Dixon, T. M., Petro, A. E., Daniel, K. W. and Collins, S. (2000):Endocrinology,141, 3630–3637.

    Article  CAS  PubMed  Google Scholar 

  37. Tkacs, N. C. and Levin, B. E. (2004):Am. J. Physiol. Regul. Integr. Comp. Physiol.,287, 1110–1115.

    Google Scholar 

  38. Tomas, E., Tsao, T.S., Saha, A. K., Murrey, H. E., Zhang, Cc. C., Itani, S. I., Lodish, H. F. and Ruderman, N. B. (2002):Proc. Natl. Acad. Sci. U S A. 99, 16309–16313.

    Article  CAS  PubMed  Google Scholar 

  39. Tulipano, G., Vergoni, A. V., Soldi, D., Muller, E. E. and Cocchi, D. (2004):J. Endocrinol.,183, 289–298.

    Article  CAS  PubMed  Google Scholar 

  40. Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L. and Friedman, J. M. (1994):Nature,372, 425–432.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Physiology and Nutrition, University of Navarra, 31008, Pamplona, Spain

    N. Pérez-Echarri, P. Pérez-Matute, J. A. Martínez, A. Marti & M. J. Moreno-Aliaga

Authors
  1. N. Pérez-Echarri
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. P. Pérez-Matute
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. J. A. Martínez
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. A. Marti
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. M. J. Moreno-Aliaga
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Pérez-Echarri, N., Pérez-Matute, P., Martínez, J.A. et al. Serum and gene expression levels of leptin and adiponectin in rats susceptible or resistant to diet-induced obesity. J. Physiol. Biochem. 61, 333–342 (2005). https://doi.org/10.1007/BF03167050

Download citation

  • Received:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF03167050

Key words

Palabras clave

Search

Navigation