The DOI matches its OpenAlex record; 3 of the 3 references it cites were found in a registry or an index.
Leptin is a metabolic signal to the reproductive system
Open accessAbstract
Leptin, a newly-discovered hormonal product of the obese (ob) gene, is expressed by adipocytes and thought to play a role in the regulation of food intake and metabolism. We tested the hypothesis that leptin signals metabolic information to the reproductive system by examining its effects on the reproductive system of ob/ob mice, which have a congenital deficiency in leptin and are infertile. We treated pair-fed males and females with leptin (50 microg twice daily, ip) or vehicle (n=10/group) for 14 days, after which the animals were bled and killed. Leptin-treated females had significantly elevated serum levels of LH, increased ovarian and uterine weights, and stimulated aspects of ovarian and uterine histology compared to controls. Leptin-treated males had significantly elevated serum levels of FSH, increased testicular and seminal vesicle weights, greater seminal vesicle epithelial cell height, and elevated sperm counts compared to controls. These results demonstrate that leptin stimulates the reproductive endocrine system in both sexes of ob/ob mice and suggest that leptin may serve as a permissive signal to the reproductive system of normal animals.
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Cites
Positional cloning of the mouse obese gene and its human homologue
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994) · Nature · doi:10.1038/372425a0 · Cited by 13,419
Abnormal splicing of the leptin receptor in diabetic mice
Lee, G.-H., Proenca, R., Montez, J. M., Carroll, K. M., Darvishzadeh, J. G., Lee, J. I., & Friedman, J. M. (1996) · Nature · doi:10.1038/379632a0 · Cited by 2,327
The role of neuropeptide Y in the antiobesity action of the obese gene product
Stephens, T. W., Basinski, M., Bristow, P. K., Bue-Valleskey, J. M., Burgett, S. G., Craft, L., Hale, J., Hoffmann, J., Hsiung, H. M., Kriauciunas, A., et al. (1995) · Nature · doi:10.1038/377530a0 · Cited by 1,498
Cited by
Effects of Recombinant Leptin Therapy in a Child with Congenital Leptin Deficiency
Farooqi, I. S., Jebb, S. A., Langmack, G., Lawrence, E., Cheetham, C. H., Prentice, A. M., Hughes, I. A., McCamish, M. A., & O'Rahilly, S. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909163411204 · Cited by 1,998
Elmquist, J. K., Elias, C. F., & Saper, C. B. (1999) · Neuron · doi:10.1016/s0896-6273(00)81084-3 · Cited by 1,160
Farooqi, I. S., Matarese, G., Lord, G. M., Keogh, J. M., Lawrence, E., Agwu, C., Sanna, V., Jebb, S. A., Perna, F., Fontana, S., et al. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215693 · Cited by 1,105
Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus
Butte, N. F. (2000) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/71.5.1256s · Cited by 826
Leptin Regulation of Neuroendocrine Systems
Ahima, R. S., Saper, C. B., Flier, J. S., & Elmquist, J. K. (2000) · Frontiers in Neuroendocrinology · doi:10.1006/frne.2000.0197 · Cited by 767
Metadata
- Authors
- Barash, I., Cheung, C. C., Weigle, D. S., Ren, H., Kabigting, E. B., Kuijper, J. L., Clifton, D. K., & Steiner, R. A.
- Venue
- Endocrinology
- Publisher
- Oxford University Press
- Published
- 1996-07-01
- Volume
- 137
- Issue
- 7
- Pages
- 3144-3147
- ISSN
- 0013-7227 (ISSN-L)
- OpenAlex
- W2122729366
- Cited by
- 1,101
- References
- 3
- FWCI
- 78.84
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Barash, I., Cheung, C. C., Weigle, D. S., Ren, H., Kabigting, E. B., Kuijper, J. L., Clifton, D. K., & Steiner, R. A. (1996). Leptin is a metabolic signal to the reproductive system. Endocrinology. https://doi.org/10.1210/en.137.7.3144
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.