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Study of the destruction mechanisms of beta pancreatic cells during the onset of Diabetes Mellitus (DM2): search for inhibition strategies of this process as well as for the recovery of insular mass in different animal models


Diabetes mellitus (DM) is defined as a syndrome of persistent hyperglycemia resulting from the lack of insulin production generally associated to increased resistance to the hormone. DM is classified as: a) insulin dependent Diabetes mellitus (IDDM) or type 1 (DM1); b) non insulin dependent Diabetes mellitus (NIDDM) or type 2 (DM2); c) Diabetes mellitus associated to other illness, or secondary DM, and d) gestational Diabetes mellitus. Almost 90% of diabetic patients belong to DM2. This disorder results from an increase in insulin resistance associated with the incapacity of the endocrine pancreas to secrete increasing amounts of insulin to compensate hyperglycemia. The maintenance of an adequate and renewable islet B-cell mass throughout life is fundamental for normoglycemia. However, until now, the mechanisms responsible for the onset of DM2 are poorly understood. In fact, the causes of accelerated B-cell destruction and the inability to restore B-cell adequately in certain individuals are unknown. To better understand the loss of islet-cells mass and functionality, in this project we will study the molecular mechanisms involved in the B-cell destruction in several experimental models, such as: diet protein restriction, obesity, dislipidemias and induced DM2. We will also analyze the molecular mechanisms involved in the increase of B-cell mass in different periods of life, such as: fetal and neonatal periods and pregnancy. Finally, we will start a program dealing with the in vitro production of insulin secreting cells derived from undifferentiated cell lines (stem cells) or from adult B-cell. (AU)

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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)
CAPPELLI, ANA PAULA G.; ZOPPI, CLAUDIO C.; SILVEIRA, LEONARDO R.; BATISTA, THIAGO M.; PAULA, FLAVIA M.; DA SILVA, PRISCILLA M. R.; RAFACHO, ALEX; BARBOSA-SAMPAIO, HELENA C.; BOSCHERO, ANTONIO C.; CARNEIRO, EVERARDO M.. Reduced glucose-induced insulin secretion in low-protein-fed rats is associated with altered pancreatic islets redox status. Journal of Cellular Physiology, v. 233, n. 1, p. 486-496, . (07/50365-4)
RIBEIRO, ROSANE A.; VANZELA, EMERIELLE C.; OLIVEIRA, CAMILA A. M.; BONFLEUR, MARIA L.; BOSCHERO, ANTONIO C.; CARNEIRO, EVERARDO M.. Taurine supplementation: involvement of cholinergic/phospholipase C and protein kinase A pathways in potentiation of insulin secretion and Ca2+ handling in mouse pancreatic islets. BRITISH JOURNAL OF NUTRITION, v. 104, n. 8, p. 1148-1155, . (07/50365-4)
AMARAL, ANDRESSA G.; RAFACHO, ALEX; DE OLIVEIRA, CAMILA A. MACHADO; BATISTA, THIAGO M.; RIBEIRO, ROSANE A.; LATORRACA, MARCIA Q.; BOSCHERO, ANTONIO C.; CARNEIRO, EVERARDO M.. Leucine Supplementation Augments Insulin Secretion in Pancreatic Islets of Malnourished Mice. PANCREAS, v. 39, n. 6, p. 847-855, . (07/50365-4)
CALEGARI, VIVIAN CRISTINE; ZOPPI, CLAUDIO CESAR; REZENDE, LUIZ FERNANDO; SILVEIRA, LEONARDO REIS; CARNEIRO, EVERARDO MAGALHAES; BOSCHERO, ANTONIO CARLOS. Endurance training activates AMP-activated protein kinase, increases expression of uncoupling protein 2 and reduces insulin secretion from rat pancreatic islets. Journal of Endocrinology, v. 208, n. 3, p. 257-264, . (07/50365-4)

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