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Cholesterol metabolism and insulin secretion in islets from hypercholesterolemic mice: possible participate of endoplasmic reticulum stress

Grant number: 12/21290-4
Support type:Scholarships abroad - Research Internship - Post-doctor
Effective date (Start): March 01, 2013
Effective date (End): February 28, 2014
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Antonio Carlos Boschiero
Grantee:Jane Cristina de Souza Sporkens
Supervisor abroad: Ira Abram Tabas
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Research place: Columbia University in the City of New York, United States  
Associated to the scholarship:11/23370-2 - Cholesterol metabolism and insulin containing granule movement in islets from hypercholesterolemic mice: Possible participate of Endoplasmic Reticulum Stress, BP.PD

Abstract

Changes in cellular cholesterol levels may contribute to B cell dysfunction. Islets from LDL receptor knockout mice (LDLR-/-) possess higher cholesterol content, showing impaired calcium handling, lower expression of proteins that promotes granule extrusion and lower insulin secretion than wild type (WT) mice. The endogenous cholesterol synthesis occurs through a series of enzymatic reactions known as the Mevalonate pathway. When activated, this pathway generates intermediary that promote post-translational modifications in proteins involved in granule extrusion process. Synthesis and accumulation of cholesterol in the endoplasmic reticulum (ER) are associated with the development of ER stress, resulting in a reduction of B cell mass and function. Based on this, the aim of this project is to evaluate whether the excess of cholesterol leads to development of endoplasmic reticulum stress triggering the Unfolded Protein Response (UPR). (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)
OZCAN, LALE; GHORPADE, DEVRAM S.; ZHENG, ZE; DE SOUZA, JANE CRISTINA; CHEN, KE; BESSLER, MARC; BAGLOO, MELISSA; SCHROPE, BETH; PESTELL, RICHARD; TABAS, IRA. Hepatocyte DACH1 Is Increased in Obesity via Nuclear Exclusion of HDAC4 and Promotes Hepatic Insulin Resistance. CELL REPORTS, v. 15, n. 10, p. 2214-2225, JUN 7 2016. Web of Science Citations: 15.
OZCAN, LALE; DE SOUZA, JANE CRISTINA; HARARI, ALP AVI; BACKS, JOHANNES; OLSON, ERIC N.; TABAS, IRA. Activation of Calcium/Calmodulin- Dependent Protein Kinase II in Obesity Mediates Suppression of Hepatic Insulin Signaling. Cell Metabolism, v. 18, n. 6, p. 803-815, DEC 3 2013. Web of Science Citations: 52.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.