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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.)

Obesity impairs lactation performance in mice by inducing prolactin resistance

Full text
Author(s):
Buonfiglio, Daniella C. [1] ; Ramos-Lobo, Angela M. [1] ; Freitas, Vanessa M. [2] ; Zampieri, Thais T. [1] ; Nagaishi, Vanessa S. [1] ; Magalhaes, Magna [2] ; Cipolla-Neto, Jose [1] ; Cella, Nathalie [2] ; Donato, Jr., Jose [1]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Cell & Dev Biol, BR-05508000 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 6, MAR 1 2016.
Web of Science Citations: 12
Abstract

Obesity reduces breastfeeding success and lactation performance in women. However, the mechanisms involved are not entirely understood. In the present study, female C57BL/6 mice were chronically exposed to a high-fat diet to induce obesity and subsequently exhibited impaired offspring viability (only 15% survival rate), milk production (33% reduction), mammopoiesis (one-third of the glandular area compared to control animals) and postpartum maternal behaviors (higher latency to retrieving and grouping the pups). Reproductive experience attenuated these defects. Diet-induced obese mice exhibited high basal pSTAT5 levels in the mammary tissue and hypothalamus, and an acute prolactin stimulus was unable to further increase pSTAT5 levels above basal levels. In contrast, genetically obese leptin-deficient females showed normal prolactin responsiveness. Additionally, we identified the expression of leptin receptors specifically in basal/myoepithelial cells of the mouse mammary gland. Finally, high-fat diet females exhibited altered mRNA levels of ERBB4 and NRG1, suggesting that obesity may involve disturbances to mammary gland paracrine circuits that are critical in the control of luminal progenitor function and lactation. In summary, our findings indicate that high leptin levels are a possible cause of the peripheral and central prolactin resistance observed in obese mice which leads to impaired lactation performance. (AU)

FAPESP's process: 10/18086-0 - Molecular basis of leptin resistance
Grantee:Jose Donato Junior
Support Opportunities: Research Grants - Young Investigators Grants
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 Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 14/11752-6 - Study of leptin functions during intrauterine and childhood stages in mice
Grantee:Angela Maria Ramos Lobo
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 15/10992-6 - Investigation of metabolic programming through different approaches
Grantee:Jose Donato Junior
Support Opportunities: 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 Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 10/07699-1 - Protease ADAMTS1 influencing breast cancer behavior and microenvironment
Grantee:Vanessa Morais Freitas
Support Opportunities: Research Grants - Young Investigators Grants