| First Author | Mounzih K | Year | 1997 |
| Journal | Endocrinology | Volume | 138 |
| Issue | 3 | Pages | 1190-3 |
| PubMed ID | 9048626 | Mgi Jnum | J:39140 |
| Mgi Id | MGI:86520 | Doi | 10.1210/endo.138.3.5024 |
| Citation | Mounzih K, et al. (1997) Leptin treatment rescues the sterility of genetically obese ob/ob males. Endocrinology 138(3):1190-3 |
| abstractText | Leptin, a hormone secreted from white adipose tissue, has been shown to normalize the body weight of ob/ob but not db/db mice as postulated by Coleman in his classical parabiosis experiments. The major effect of leptin is therefore to decrease food intake, thus resulting in a breakdown of fat stores. Recently, we have suggested that leptin plays a role in reproductive physiology based on the observation that leptin treatment but not food restriction rescues the sterility of ob/ob females. In the present communication, we treated sterile ob/ob males with leptin and asked whether fertility could be induced, thus selecting their reproductive ability as the endpoint of the experiment. Our results show that all food-restricted ob/ob males are unable to impregnate normal C57BL/6J females. However, all leptin-treated ob/ob males fertilized normal females mice that carried out normal pregnancies and deliveries, demonstrating that the reproductive capacity of ob/ob males was corrected only with leptin treatment. Furthermore, reproductive indices such as testicular weight and histology are normalized in leptin-treated animals. Therefore, as in ob/ob females, leptin plays a significant role in the male mouse reproductive pathways. |
