Crosstalk between leptin and prolactin in the brain: possible mechanism of metabolic changes during pregnancy

• Grant number: 13/16374-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: September 01, 2013
• End date: August 31, 2014
• Field of knowledge: Biological Sciences - Physiology
• Principal Investigator: Jose Donato Junior
• Grantee: Vanessa Sayuri Nagaishi
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 10/18086-0 - Molecular basis of leptin resistance, AP.JP

Abstract

During pregnancy, rodents and humans show increased food intake and adiposity. Nevertheless, circulating leptin concentration is increased in this situation as well as the hypothalamic expression of the suppressor of cytokine signaling 3 (SOCS3). Thus, pregnancy is an interesting model of leptin resistance because its transitory nature. However, the molecular mechanisms which are responsible for leptin resistance during pregnancy are unknown. A hyper-activation of the prolactin receptor (PrlR) is a potential factor which may be associated with leptin resistance observed in pregnancy. PrlR can be activated by placental lactogens as well. This receptor, just like the leptin receptor (LepR), can induce the phosphorylation of the signal transducer and activators of transcription (STATs) increasing the expression of SOCS3, which in turn can inhibit signaling of LepR. This hypothesis is plausible only if LepR and PrlR are expressed in the same neuronal population. This research aims to identify the brain areas which have cells that co-express prolactin and leptin receptors.

Scientific publications

(4)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

BUONFIGLIO, DANIELLA C.; RAMOS-LOBO, ANGELA M.; FREITAS, VANESSA M.; ZAMPIERI, THAIS T.; NAGAISHI, VANESSA S.; MAGALHAES, MAGNA; CIPOLLA-NETO, JOSE; CELLA, NATHALIE; DONATO, JR., JOSE. Obesity impairs lactation performance in mice by inducing prolactin resistance. SCIENTIFIC REPORTS, v. 6, MAR 1 2016. (10/18086-0, 13/16374-7, 14/11752-6, 15/10992-6, 12/15517-6, 10/07699-1)

DA SILVA, REGINA P.; ZAMPIERI, THAIS T.; PEDROSO, JOAO A. B.; NAGAISHI, VANESSA S.; RAMOS-LOBO, ANGELA M.; FURIGO, ISADORA C.; CAMARA, NIELS O.; FRAZAO, RENATA; DONATO, JR., JOSE. Leptin Resistance Is Not the Primary Cause of Weight Gain Associated With Reduced Sex Hormone Levels in Female Mice. Endocrinology, v. 155, n. 11, p. 4226-4236, NOV 2014. (13/00801-3, 10/18086-0, 12/12202-4, 13/16374-7, 12/02270-2, 12/15517-6, 13/21722-4)

NAGAISHI, V. S.; CARDINALI, L. I.; ZAMPIERI, T. T.; FURIGO, I. C.; METZGER, M.; DONATO, JR., J.. POSSIBLE CROSSTALK BETWEEN LEPTIN AND PROLACTIN DURING PREGNANCY. Neuroscience, v. 259, p. 71-83, FEB 14 2014. (12/15517-6, 12/02388-3, 10/18086-0, 13/16374-7)

FURIGO, ISADORA C.; KIM, KI WOO; NAGAISHI, VANESSA S.; RAMOS-LOBO, ANGELA M.; DE ALENCAR, AMANDA; PEDROSO, JOAO A. B.; METZGER, MARTIN; DONATO, JR., JOSE. Prolactin-sensitive neurons express estrogen receptor-alpha and depend on sex hormones for normal responsiveness to prolactin. Brain Research, v. 1566, p. 47-59, MAY 30 2014. (13/21722-4, 12/02388-3, 10/18086-0, 13/16374-7)