While Tinkering With the β-Cell… Metabolic Regulatory Mechanisms and New Therapeutic Strategies
American Diabetes Association Lilly Lecture, 2001
- From the Touchstone Center for Diabetes Research and Departments of Biochemistry & Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
Abstract
A common feature of the two major forms of human diabetes is the partial or complete loss of insulin secretion from β-cells in the pancreatic islets of Langerhans. In this article, we review the development of a set of tools for studying β-cell biology and their application to understanding of fuel-mediated insulin secretion and enhancement of β-cell survival. Insights into these basic issues are likely to be useful for the design of new drug and cell-based diabetes therapies.
Footnotes
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Address correspondence and reprint requests to Christopher B. Newgard, Sarah W. Stedman Center for Nutritional Studies, Department of Pharmacology & Cancer Biology, DUMC 3813, Duke University Medical Center, Durham, NC 27710. E-mail: newga002{at}mc.duke.edu.
Received for publication 13 March 2002 and accepted 19 March 2002.
DMM, dimethylmalate; GSIS, glucose-stimulated insulin secretion; IFN-γ, interferon-γ; IL-1β, interleukin-1β; iNOS, inducible nitric oxide synthase; NF-κB, nuclear factor κB; NMR, nuclear magnetic resonance; PAA, phenylacetic acid; PBMC, peripheral blood mononuclear cell; PC, pyruvate carboxylase; PDH, pyruvate dehydrogenase; PEPCK, phosphoenolpyruvate carboxykinase; RDA, representational difference analysis; TCA, tricarboxylic acid.
- DIABETES
