Secretory pattern of leptin and LH during lactational amenorrhoea in breastfeeding normal and polycystic ovarian syndrome women

• Published in: Human reproduction (Oxford) 2001-02, Vol.16 (2), p.244-249
• Main Authors: Sir-Petermann, T., Recabarren, S.E., Lobos, A., Maliqueo, M., Wildt, L.
• Format: Article
• Language: English
• Subjects: Adult; Amenorrhea - physiopathology; Biological and medical sciences; Breast Feeding; Case-Control Studies; Female; Female genital diseases; Gynecology. Andrology. Obstetrics; Humans; lactation; Lactation - physiology; leptin; Leptin - blood; Leptin - metabolism; Luteinizing Hormone - blood; Luteinizing Hormone - metabolism; Medical sciences; polycystic ovarian syndrome; Polycystic Ovary Syndrome - physiopathology; Postpartum Period; Tumors
• ISSN: 0268-1161; 1460-2350; 1460-2350
• DOI: 10.1093/humrep/16.2.244

Several studies have suggested that leptin modulates hypothalamic–pituitary–gonadal axis function. A synchronicity of LH and leptin pulses has been described in healthy women and in patients with polycystic ovarian syndrome (PCOS), suggesting that leptin may modulate the episodic secretion of LH. The aim of the present investigation was to assess the episodic fluctuations of circulating LH and leptin during lactational amenorrhoea in fully breastfeeding normal and PCOS women at 4 and 8 weeks postpartum, in order to establish LH–leptin interactions in the reactivation of the gonadal axis during this period. Six lactating PCOS patients and six normal lactating women of similar age and body mass index were studied. During a 12 h period on the 4th and 8th weeks postpartum, blood samples were collected at 10 min intervals for 12 h (22:00–10:00). Serum LH and leptin concentrations were measured in all samples. For pulse analysis, the cluster algorithm was used. To detect an interaction between LH and leptin pulses, an analysis of co-pulsatility was employed. LH concentrations tended to increase in both groups between the 4th and 8th weeks postpartum; however, serum leptin concentrations were not modified. Leptin pulse frequencies were similar at the 4th and 8th weeks postpartum, and did not differ between groups. Moreover, leptin pulse frequency was higher than LH pulse frequency in both groups, and in the two study periods. There was no synchronicity between LH and leptin pulses, and there were no increments in leptin concentration during the night. The fact that leptin concentrations were not modified and no synchronicity between LH and leptin pulses was observed suggests that, during lactational amenorrhoea, circulating leptin is probably not involved as a primary signal in promoting the reactivation of pulsatile LH secretion.