Established in 1977 and last renewed in 1985, this DRTC has continued to augment diabetes-related research and training at Indiana University using Core facilities, pilot project funding, research training programs, enrichment functions and by facilitating collaboration. Our research base has expanded and is characterized by particular strengths in cellular and molecular biology, human research in adult and pediatric metabolism, diabetic complications, and health care delivery research. This application describes our research base, its increase in both depth and scope using the resources of the DRTC, and describes research progress since 1985. We propose continuation of three current Cores: MOLECULAR BIOLOGY AND PROTEIN ANALYSIS (which enhances diabetes research at Purdue and Indiana University), IMMUNOLOGICAL SERVICES, AND BIOSTATISTICS AND EPIDEMIOLOGY. Each Core has successfully met its objectives, and expansion to meet increased demands for services is proposed. The proposal contains a summary of the pilot Project progress and requests continuation. The D & E component reviews and summarizes our progress since 1985. We also propose to continue three training cores: MODEL DIABETES UNIT (MDU), OUTREACH and EDUCATIONAL DEVELOPMENT AND EVALUATION (EDEC). In response to a greatly expanded base in human metabolism a new MDU subcore, the HUMAN BIOLOGY CORE, is proposed to promote and augment human research by both clinical and basic investigators. One continuing and give exciting new training projects are proposed; three dealing with intensive metabolic control in children and adolescents (which could be particularly relevant should the results of the DCCT be positive), two dealing with treatment of NIDDM in low SDS African Americans and one dealing with transferring diabetes standards to practicing physicians. We are also proposing the EDEC to develop and study application of hypermedia technology to the training of physicians.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Comprehensive Center (P60)
Project #
5P60DK020542-20
Application #
2015996
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Fradkin, Judith E
Project Start
1977-09-01
Project End
1997-11-30
Budget Start
1996-12-01
Budget End
1997-11-30
Support Year
20
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Indiana University-Purdue University at Indianapolis
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
005436803
City
Indianapolis
State
IN
Country
United States
Zip Code
46202
Hannon, Tamara S; Kirkman, M S; Patel, Yash R et al. (2014) Profound defects in ?-cell function in screen-detected type 2 diabetes are not improved with glucose-lowering treatment in the Early Diabetes Intervention Program (EDIP). Diabetes Metab Res Rev 30:767-76
Patel, Y R; Kirkman, M S; Considine, R V et al. (2013) Effect of acarbose to delay progression of carotid intima-media thickness in early diabetes. Diabetes Metab Res Rev 29:582-91
Kirkman, M Sue; Shankar, R Ravi; Shankar, Sudha et al. (2006) Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes: the Early Diabetes Intervention Program. Diabetes Care 29:2095-101
Wilson, Wayne A; Wang, Zhong; Roach, Peter J (2005) Regulation of yeast glycogen phosphorylase by the cyclin-dependent protein kinase Pho85p. Biochem Biophys Res Commun 329:161-7
Hermel, Evan; Hart, Andrew J; Gunduz, Irfan et al. (2004) Polymorphism and conservation of the genes encoding Qa1 molecules. Immunogenetics 56:639-49
Pederson, Bartholomew A; Wilson, Wayne A; Roach, Peter J (2004) Glycogen synthase sensitivity to glucose-6-P is important for controlling glycogen accumulation in Saccharomyces cerevisiae. J Biol Chem 279:13764-8
Wilson, Wayne A; Hughes, William E; Tomamichel, Wendy et al. (2004) Increased glycogen storage in yeast results in less branched glycogen. Biochem Biophys Res Commun 320:416-23
Duan, Chaojun; Li, Minghua; Rui, Liangyou (2004) SH2-B promotes insulin receptor substrate 1 (IRS1)- and IRS2-mediated activation of the phosphatidylinositol 3-kinase pathway in response to leptin. J Biol Chem 279:43684-91
Shankar, Sudha S; Mirzamohammadi, Bahram; Walsh, James P et al. (2004) L-carnitine may attenuate free fatty acid-induced endothelial dysfunction. Ann N Y Acad Sci 1033:189-97
Thurmond, Debbie C; Gonelle-Gispert, Carmen; Furukawa, Megumi et al. (2003) Glucose-stimulated insulin secretion is coupled to the interaction of actin with the t-SNARE (target membrane soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein) complex. Mol Endocrinol 17:732-42

Showing the most recent 10 out of 151 publications