Abstract
Leptin, the product of the obese gene first identified in mice, restores fertility in obese mice, and accelerates puberty in mice. We hypothesized that leptin’s putative role in reproduction may extend to pregnancy and lactation. Leptin levels were determined inMyotis lucifugus, the little brown bat, a free-ranging mammal with a seasonal breeding cycle. The present study shows that plasma levels of leptin progressively rise during pregnancy, supporting a potential role for leptin in the maintenancy of pregnancy. In contrast, leptin was significantly lower during lactation, a time when most mammals, including bats, demonstrate reduced fertility. In addition to its possible roles in reproduction, leptin appears important in regulation of energy balance.M. lucifugus spontaneously fasts for up to 16 h each day during the active season, which allowed us to test the hypothesis that acute fasting was associated with decreased leptin. Leptin was significantly lower in fasted (lactating) bats, compared to those that recently returned from nightly foraging. Although postprandial lactating bats had a significantly higher fat index than fasted bats, plasma leptin and body fat were not significantly correlated, and were only weakly correlated (r 2=0.26) when both pregnant and lactating females were included in the analysis. Similar changes during pregnancy, lactation, and the daily feeding cycle were observed in the hypothalamic neuropeptide, corticotropin-releasing hormone (CRH), which is believed to play an important role in energy balance and reproduction. By contrast, neuropeptide Y (NPY) increased during pregnancy but did not change during fasting. These results suggest that leptin’s putative role in reproduction may extend to pregnancy and lactation, and that spontaneous, acute fasting results in decreased circulating levels of leptin inM. lucifugus.
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Stanley, B. G., Lanthier, D., Chin, A. S., and Leibowitz, S. F. (1989).Brain Res. 501, 32–36.
Zarjevski, N., Cusin, I., Vettor, R., Rohner-Jeanrenaud, F., and Jeanrenaud B. (1993).Endocrinology 133, 1753–1758.
Billington, C. J., Briggs, J. E., Harker, S., Grace, M., and Levine, A. S. (1994).Am. J. Physiol. 266, R1765-R1770.
Sanacora, G., Kershaw, M., Finkelstein, J. A., and White, J. (1990).Endocrinology 127, 730–737.
Erickson, J. C., Clegg, K. E., and Palmiter, R. D. (1996).Nature 381, 415–417.
Erickson, J. C., Hollopeter G., and Palmiter R. D. (1996).Science 274, 1704–1707.
Rothwell, N. J. (1990).Neurosci. Biobehav. Rev. 14, 263–271.
Rohner-Jeanrenaud, F., Walker, C. D., Greco-Perotto, R., and Jeanrenaud, B. (1989).Endocrinology 124, 733–739.
Ahima, R. S., Prabakaran, D., Mantzoros, C., Qu, D., Lowell, B., Maratos-Flier, E., and Flier, J. S. (1996).Nature 382, 250–252.
Schwartz, M. W., Baskin, D. G., Bukowski, T. R., Kuijper, J. L., Foster, D., Lasser, G., Prunkard, D. E., Porte, D., Jr., Woods, S. C., Seeley, R. J., and Weigle, D. S. (1996).Diabetes 45, 531–535.
Mercer, J. G., Hoggard, N., Williams, L. M., Lawrence, C. B., Hannah, L. T., Morgan, P. J., and Trayhurn, P. (1996).J. Neuroendocrinology 8, 733–735.
Smith, F. J., Campfield, L. A., Moschera, J. A., Bailon, P. S., and Burn, P. (1996).Nature 382, 307.
Stephens, T. W., Basinski, M., Bristow, P. K., Bue-Valleskey, J. M., Burgett, S. G., Craft, L., Hale, J., Hoffmann, J., Hsuing, H. M., Kriauciunas, A., MacKellar, W., Rosteck, P. R., Jr, Schoner, B., Smith, D., Tinsley, F. C., Zhang, X.-Y., and Heiman, M. (1995).Nature.377, 530–532.
Campfield, L. A., Smith, F. J., Guisez, Y., Devos, R., and Burn, P. (1995).Science 269, 546–549.
Halaas J. L., Gajiwala, K. S., Maffei, M., Cohen, S. L., Chait, B. T., Rabinowitz, D., Lallone, R. L., Burley, S. K., and Friedman, J. M. (1995).Science 269, 543–546.
Chehab, F. F., Lim, M. E., and Lu, R. (1996).Nat. Genet. 12, 318–320.
Chehab, F. F., Mounzih, K., Lu, R., and Lim, M. E. (1997).Science 275, 88–90.
Anthony, E. and Kunz, T. H. (1977).Ecology 58, 775–786.
Schwartz, M. W., Peskind, E., Raskind, M., Boyko, E. J., and Porte, D., Jr. (1996).Nat. Med. 2, 589–593.
Ma, Z., Gingerich, R. L., Santiago, J. V., Klein, S., Smith, C. H., and Landt, M. (1996).Clin. Chem. 42, 942–946.
Burnett, C. D. and Kunz, T. H. (1982).J. Mammology 63, 33–41.
Bronson, F. H. (1989).Mammalian Reproductive Biology. University of Chicago Press, Chicago.
Sinha, M. K., Ohannesian, J. P., Heiman, J. L., Kriauciunas, A., Stephens, T. W., Magosin, S., Marco, C., and Caro, J. F. (1996).J. Clin. Invest. 97, 1344–1347.
Freiderich, R. C., Lollman, B., Hamann, A., Napolitano-Rosen, A., Kahn, B. B., Lowell, B. B., and Flier, J. S. (1995).J. Clin. Invest. 96, 1658–1663.
Kalra, S. P., Dube, M. G., Sahu, A., Phelps, C. P., and Kalra, P. S. (1991).Proc. Natl. Acad. Sci. USA 88, 10,931–10,935.
Laemle, L. K and Cotter, J. R. (1992).J. Comp. Neurol. 316, 447–458.
Widmaier, E. P., Harmer, T. L., Sulak, A. M., and Kunz, T. H. (1994).J. Exp. Zool. 269, 442–449.
Widmaier, E. P., Gornstein, E. R., Hennessey, J. L., Bloss, J. M., Greenberg, J. A., and Kunz, T. H. (1996).Am. J. Physiol. 271, R1101-R1106.
Kurta, A., Bell, G. P., and Nagy, K. A. (1989).Can. J. Zool. 67, 2468–2472.
Kunz, T. H. and Kurta, A. (1988). In:Ecological and Behavioral Methods for the Study of Bats. Kunz, T. H. (ed.), Smithsonian Institution Press: Washington, DC, pp. 1–30.
Widmaier, E. P., Lim, A. L., and Vale, W. (1989).Endocrinology 124, 583–590.
Kunz, T. H., Burnett, C. D., and Wrazen, J. R. (1997).Ecoscience, in press.
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Widmaier, E.P., Long, J., Cadigan, B. et al. Leptin, corticotropin-releasing hormone (CRH), and neuropeptide Y (NPY) in free-ranging pregnant bats. Endocr 7, 145–150 (1997). https://doi.org/10.1007/BF02778135
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DOI: https://doi.org/10.1007/BF02778135