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Diabetes, Vol 37, Issue 10 1311-1315, Copyright © 1988 by American Diabetes Association

ARTICLES

Descriptive and mechanistic considerations of interleukin 1 and insulin secretion

ML McDaniel, JH Hughes, BA Wolf, RA Easom and JW Turk
Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110.

Insulin-dependent diabetes mellitus (IDDM) may be mediated in part by an autoimmune mechanism, as suggested by associated cytologic and serologic phenomena, e.g., insulitis, beta-cell necrosis, and the presence of both islet cell and insulin antibodies. Immunological approaches to the prediction and intervention in the progression of beta-cell destruction in this disease are under evaluation. A recent hypothesis is that cytokines, including interleukin 1 (IL-1), play causative roles in such autoimmune processes. Several studies have convincingly demonstrated that IL-1 is a potent modulator of beta-cell function and can potentiate or inhibit glucose-induced insulin secretion, depending on the concentration and length of exposure to IL-1. IL-1 alone or in concert with other cytokines is cytotoxic to beta-cells. The cellular mechanisms responsible for the potent effects of IL-1 on the beta-cell are unknown and just beginning to emerge. Although speculative at this time, this perspective delineates cellular mechanisms that are likely to represent possible primary sites for the IL-1 action on beta-cells. A mechanistic understanding of the effects of IL-1 on the beta-cell may clarify its role in modulating insulin release in vivo or yield insight into the pathogenesis of IDDM.
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This article has been cited by other articles:


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Z. Ma, S. Ramanadham, J. A. Corbett, A. Bohrer, R. W. Gross, M. L. McDaniel, and J. Turk
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[Abstract] [Full Text] [PDF]


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Copyright © 1988 by the American Diabetes Association.