Abstract

We plan to evaluate the control of secretion of somatostatin, glucagon, and insulin using the perfused pancreas of rat, dog, and chicken. Morphological studies will be undertaken to search for evidence of cell-cell interactions in islets and to characterize regional variation of structure of the endocrine pancreas. Work on somatostatin biosynthesis will be carried out to determine rates of synthesis and how these correlate with secretory events. We will also study islet growth, development, and response to injury in the endocrine pancreas of neonatal rats. Our hope is that these studies will enhance our understanding of the pathophysiology of diabetes mellitus.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK035449-03
Application #
3233784
Study Section
(SSS)
Project Start
1984-09-01
Project End
1987-08-31
Budget Start
1986-09-01
Budget End
1987-08-31
Support Year
3
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
Joslin Diabetes Center
Department
Type
DUNS #
071723084
City
Boston
State
MA
Country
United States
Zip Code
02215

  Publications

Goldfine, Allison B; Patti, Mary Elizabeth (2015) New lessons from gastric bypass: Impact of glucose-independent islet function. Obesity (Silver Spring) 23:1942-3
Lopez-Avalos, Maria D; Duvivier-Kali, Valerie F; Xu, Gang et al. (2006) Evidence for a role of the ubiquitin-proteasome pathway in pancreatic islets. Diabetes 55:1223-31
Weir, Gordon C; Bonner-Weir, Susan (2004) Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes 53 Suppl 3:S16-21
Weir, Gordon C (2004) Can we make surrogate beta-cells better than the original? Semin Cell Dev Biol 15:347-57
Patane, Giovanni; Kaneto, Hideaki; Toschi, Elena et al. (2003) Induction of Mad expression leads to augmentation of insulin gene transcription. Biochem Biophys Res Commun 303:1199-208
Laybutt, D Ross; Glandt, Mariela; Xu, Gang et al. (2003) Critical reduction in beta-cell mass results in two distinct outcomes over time. Adaptation with impaired glucose tolerance or decompensated diabetes. J Biol Chem 278:2997-3005
Kaneto, Hideaki; Xu, Gang; Fujii, Nobuharu et al. (2002) Involvement of c-Jun N-terminal kinase in oxidative stress-mediated suppression of insulin gene expression. J Biol Chem 277:30010-8
Laybutt, D Ross; Weir, Gordon C; Kaneto, Hideaki et al. (2002) Overexpression of c-Myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes. Diabetes 51:1793-804
Laybutt, D Ross; Kaneto, Hideaki; Hasenkamp, Wendy et al. (2002) Increased expression of antioxidant and antiapoptotic genes in islets that may contribute to beta-cell survival during chronic hyperglycemia. Diabetes 51:413-23
Laybutt, D Ross; Sharma, Arun; Sgroi, Dennis C et al. (2002) Genetic regulation of metabolic pathways in beta-cells disrupted by hyperglycemia. J Biol Chem 277:10912-21

Showing the most recent 10 out of 80 publications