Lack of cross-desensitization between leptin and prolactin signaling pathways despite the induction of suppressor of cytokine signaling 3 and PTP-1B

• DOI: 10.1677/joe-07-0321
• Publication Date: 2007-10-19T18:39:10Z
• Authors: A F Roy; Y Benomar; V Bailleux; C M Vacher; A Aubourg; A Gertler; J Djiane; M Taouis
• Keywords: Leptin receptor

Hyperprolactinemia and hyperleptinemia occur during gestation lactation with marked hyperphagia associated leptin resistance. Prolactin (PRL) induces the expression of orexigenic neuropeptide Y (NPY) through activation JAK-2/STAT-3 signaling pathway in hypothalamic paraventricular nucleus (PVN) leading to hyperphagia. PRL may also act inhibition anorexigenic effect via induction suppressor cytokine 3 (SOCS-3). This paper aimed co-localize (PRL-R) (ObRb) receptors hypothalamus female rats investigate possible cross-desensitization between PRL-R ObRb. We showed that: 1) ObRb are expressed PVN co-localized same neurons; 2) lactating females failed activate pathway; 3) Chinese Hamster Ovary (CHO) stably co-expressing ObRb, overexposure did not affect but totally abolished PRL-dependent STAT-5 phosphorylation. The produces similar results strong alteration leptin-dependent STAT-3 phosphorylation, whereas was affected; 4) CHO-ObRb/PRL-R cells or negative regulators SOCS-3 PTP-1B. Thus, we conclude that these specifically inducer for instance, induced by will vice versa. Finally, lack PURL-R suggests observed be attributed a direct on NPYexpression, is most likely exacerbated physiological resistance state.