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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1996-11-29
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pubmed:abstractText |
Autoimmune processes are involved in pancreatic beta-cell destruction in type 1 diabetes. Autoantibodies including islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA), and antibodies directed against the 37/ 40 K antigen appear in the circulation years before clinical onset and permit increasingly precise disease prediction. A cellular immune response causes pancreatic infiltration, while macrophages and Th-cells appear to be implicated-via local release of cytokines-in beta-cell destruction. Generation of free radicals, DNA strand breaks, activation of the enzyme poly (ADP-ribose) polymerase (PARP), and depletion of intracellular nicotinamide adenine dinucleotide (NAD) appear to be common factors in beta-cell death, whether mediated by oxygen radicals, nitric oxide, or streptozotocin. Nicotinamide, a soluble B group vitamin which offers protection against these toxic stimuli, is at high doses a free radical scavenger, a potent inhibitor of PARP, and protects against depletion of intracellular NAD. A sound scientific rationale therefore exists for its use in human prediabetes, and promising pilot studies have been performed in ICA-positive first-degree relatives and school children. No serious side effects have been reported from its use at the doses proposed in man or other species. There is therefore a sound case for submitting this agent to a controlled clinical trial.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0301-0163
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
45 Suppl 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
39-43
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pubmed:dateRevised |
2005-11-16
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pubmed:meshHeading | |
pubmed:year |
1996
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pubmed:articleTitle |
Molecular mechanisms of beta-cell destruction in IDDM: the role of nicotinamide.
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pubmed:affiliation |
Department of Diabetes and Metabolism, St Bartholomew's Hospital, London, UK.
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pubmed:publicationType |
Journal Article,
Review
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