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2008-D-027-FEL - Abstract

Grant Information

Grant
2008-D-027-FEL
Diabetes - Fellowship
Title
Role of Proteosomal Ubiquitin Pathway in Endoplasmic Reticulum Stress in Beta Cells
Investigator
Safia Costes, PhD
Institution
UCLA
Medicine/Endocrinology
Funding Status
  • Completed
  • 3 years, $60,000 per year
  • 7/1/2008 to 6/30/2011

Abstract

2008-D-027-FEL - Abstract
Brief Summary
"The Role of Proteosomal Ubiquitin Pathway in Endoplasmic Reticulum Stress in Beta Cells"

In health, the level of glucose in blood is tightly controlled. This control is implemented by a feedback loop. In brief, if the blood glucose increases then this stimulates release of the hormone insulin by pancreatic beta-cells and the insulin works at the level of the liver and muscle to bring the blood glucose back down to normal.

For this system to work there needs to be sufficient beta-cells present to secrete the required amount of insulin. In both type 1 and 2 diabetes there are insufficient beta-cells. In type 2 diabetes (T2DM), the cause of beta-cell loss is unknown, but the islet pathology is very comparable to that in people with neurodegenerative diseases such as Alzheimer’s or Parkinson’s diseases. In those diseases, the mechanisms that lead to cell death have been found to relate to the accumulation of toxic aggregates of proteins. A very similar mechanism seems to be important in T2DM.

In this project, the focus is on establishing to what extent the systems (called ubiquitin-proteasome system and autophagy) for eliminating toxic protein aggregates are dysfunctional in T2DM. These pathways involved in protein degradation have been shown to be dysfunctional in neurons in neurodegenerative diseases. Our studies suggest that there appears to be abnormalities in these systems in beta-cells of subjects with T2DM. Establishing what these abnormalities are, and how they influence cell killing, are the basis of this research.

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