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Endocrine pancreas plasticity of mice offspring after maternal treatment with glucocorticoid during late gestation

Grant number: 16/23140-0
Support Opportunities:Scholarships in Brazil - Doctorate
Effective date (Start): July 01, 2017
Effective date (End): May 31, 2021
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Acordo de Cooperação: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Antonio Carlos Boschiero
Grantee:Cristiane dos Santos
Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass, AP.TEM
Associated scholarship(s):19/10543-8 - Investigation on epigenetic mechanisms involved in islet dysfunction by prenatal glucocorticoid treatment, BE.EP.DR


The pancreatic ² cells have ample capacity to adapt to numerous physiological demands via cellular processes of proliferation, transdifferentiation, hypertrophy and apoptosis. The neonatal period is a stage of high plasticity of the endocrine pancreas, however the mechanisms involved in this process are not fully understood. The hepatocyte nuclear factor 4± (HNF4±) is a transcription factor involved in the regulation of glucose-stimulated insulin secretion and proliferation of pancreatic cells. Thus, HNF4± may be involved in the plasticity of the endocrine pancreas. Epigenetic studies have investigated the impact of exposure to glucocorticoids (GC) during intrauterine period on the endocrine pancreas development and point to glucose intolerance as a metabolic outcome in adult offspring. During the early postnatal period there is high cell plasticity and the endocrine pancreas of rodents are able to recover the ² cell mass after neonatal insult. Thus, we hypothesize that the ability of the endocrine pancreas to recover the ² cell mass after exposure to streptozotocin will be reduced in the adult offspring of mice exposed to GC in late gestation. With this strategy to promote reduction in ² cells mass in newborn animals, in which cell plasticity is quite pronounced, we will investigate the main molecular targets involved in the plasticity of ² cells and how vulnerable they are in offspring exposed to GC in critical periods of development. For this, we will monitor ² and ± cells mass throughout growth up to adult period and evaluate gene expression and methylation profile of the main transcription factors involved in the development of the endocrine pancreas, as well as the involvement of HNF4-± in the cell growth process through the use of ±-HNF4 -/- animals. (AU)

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Scientific publications
(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)
DOS SANTOS, CRISTIANE; RAFACHO, ALEX; FERREIRA, SANDRA MARA; VETTORAZZI, JEAN FRANCIESCO; DOS REIS ARAUJO, THIAGO; MATEUS GONCALVES, LUCIANA; RUHRMANN, SABRINA; BACOS, KARL; LING, CHARLOTTE; BOSCHERO, ANTONIO CARLOS; et al. Excess of glucocorticoids during late gestation impairs the recovery of offspring's beta-cell function after a postnatal injury. FASEB JOURNAL, v. 35, n. 8, . (19/10543-8, 16/23140-0, 15/12611-0)
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
SANTOS, Cristiane dos. The excess of glucocorticoid, during gestation in mice, impairs the recovery of offspring's pancreatic beta-cells. 2021. Doctoral Thesis - Universidade Estadual de Campinas (UNICAMP). Instituto de Biologia Campinas, SP.

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