Increasing evidence suggests that insulin dependent diabetes is the result of one or more defects involving the pancreatic beta cells. The objective of this project is to elucidate further the physiology, biochemistry and morphology of pancreatic islet cells, and to determine the possible role of immune factors in causing beta cell damage in diabetes. Three areas will be investigated: 1) continuous clonal lines of rat pancreatic islet cells developed in our laboratory will be further characterized. These cells will be used in a variety of studies including preparation of somatic cell hybrids and examination of the role of paracrine influences in regulating insulin secretion; 2) the etiology of insulitis and beta cell damage in the spontaneously diabetic BB rat will be studied. The role of cell and antibody mediated cytotoxicity will be examined using chromium-51 labeled beta cell targets and lymphocyte effector cells from BB rats with acute insulitis; 3) the possible role of DNA methylation in controlling insulin gene expression will be examined.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK030846-07
Application #
3229694
Study Section
Metabolism Study Section (MET)
Project Start
1981-07-01
Project End
1988-01-31
Budget Start
1987-02-01
Budget End
1988-01-31
Support Year
7
Fiscal Year
1987
Total Cost
Indirect Cost
Name
University of Massachusetts Medical School Worcester
Department
Type
Schools of Medicine
DUNS #
660735098
City
Worcester
State
MA
Country
United States
Zip Code
01655
Clark, S A; Burnham, B L; Chick, W L (1990) Modulation of glucose-induced insulin secretion from a rat clonal beta-cell line. Endocrinology 127:2779-88
Clark, S A; Chick, W L (1990) Islet cell culture in defined serum-free medium. Endocrinology 126:1895-903