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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

POSSIBLE CROSSTALK BETWEEN LEPTIN AND PROLACTIN DURING PREGNANCY

Full text
Author(s):
Nagaishi, V. S. [1] ; Cardinali, L. I. [1] ; Zampieri, T. T. [1] ; Furigo, I. C. [1] ; Metzger, M. [1] ; Donato, Jr., J. [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Neuroscience; v. 259, p. 71-83, FEB 14 2014.
Web of Science Citations: 34
Abstract

Rodents exhibit leptin resistance and high levels of prolactin/placental lactogens during pregnancy. A crosstalk between prolactin and leptin signaling has been proposed as a possible mechanism to explain the changes in energy balance during gestation. However, it remains unclear if specific neuronal populations co-express leptin and prolactin receptors. Therefore, our present study was undertaken to identify in the mouse brain prolactin-responsive cells that possibly express the leptin receptor (LepR). In addition, we assessed the leptin response in different brain nuclei of pregnant and nulliparous mice. We used a LepR-reporter mouse to visualize LepR-expressing cells with the tdTomato fluorescent protein. Prolactin-responsive cells were visualized with the immunohistochemical detection of the phosphorylated form of the signal transducer and activator of transcription-5 (pSTAT5-ir). Notably, many neurons that co-expressed tdTomato and pSTAT5-ir were observed in the medial preoptic area (MPA, 27-48% of tdTomato cells), the retrochiasmatic area (34-51%) and the nucleus of the solitary tract (NTS, 16-24%) of prolactin-treated nulliparous mice, pregnant mice and prolactin-treated leptin-deficient (ob/ob) mice. The arcuate nucleus of the hypothalamus (8-22%), the medial tuberal nucleus (11-15%) and the ventral premammillary nucleus (4-10%) showed smaller percentages of double-labeled cells among the groups. Other brain nuclei did not show significant percentages of neurons that co-expressed tdTomato and pSTAT5-ir. Late pregnant mice exhibited a reduced leptin response in the MPA and NTS when compared with nulliparous mice; however, a normal leptin response was observed in other brain nuclei. In conclusion, our findings shed light on how the brain integrates the information conveyed by leptin and prolactin. Our results corroborate the hypothesis that high levels of prolactin or placental lactogens during pregnancy may directly interfere with LepR signaling, possibly predisposing to leptin resistance. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved. (AU)

FAPESP's process: 10/18086-0 - Molecular basis of leptin resistance
Grantee:Jose Donato Junior
Support type: Research Grants - Young Investigators Grants
FAPESP's process: 12/02388-3 - Topography and transmitter phenotype of the projections between the lateral habenula, the rostromedial tegmental nucleus and the dorsal raphe nucleus in the rat
Grantee:Martin Andreas Metzger
Support type: Regular Research Grants
FAPESP's process: 12/15517-6 - Involvment of molecular factors in metabolic changes during pregnancy: role of SOCS3
Grantee:Thais Tessari Zampieri
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 13/16374-7 - Crosstalk between leptin and prolactin in the brain: possible mechanism of metabolic changes during pregnancy
Grantee:Vanessa Sayuri Nagaishi
Support type: Scholarships in Brazil - Scientific Initiation