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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1998-12-15
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pubmed:abstractText |
Insulin action starts with binding to a membrane receptor (insulin receptor-tyrosine kinase) and with activating an insulin receptor substrate 1 (IRS-1) and substrate 2 (IRS-2). Insulin receptors interact at least with three cascade reactions, phosphorylating G proteins and IRS-1, that activate PLC "ras" and PI-3-K. NIDDM can be defined as a disease caused by defective transduction of insulin signals and IR as a complex phenotype manifesting itself, emphasized by individual and environmental factors, in the cellular systems of signal transduction. IRS is a syndrome characterized by NIDDM, hypertension, visceral obesity, CHD: the X syndrome. Up to day the described mutations of the insulin-receptor gene are rare (e.g. the leprechaunism): genetic IR. Obesity is the principal cause of IR by receptorial and post-receptorial defects: metabolic IR. The obese skeletal muscle shows a reduction of insulin receptor and IRS-1 phosphorylation and of PI-3-K activation; the scarce expression of these proteins would determine the muscular IR. IR is a pattern of essential hypertension. Hypertension, dyslipidemia and abnormality of glucose metabolism are linked by IR. The so called high erythrocyte Na(+)-Li+ counter-transport is a new biochemical marker for IR and hypertension. These drugs can reduce IR: metformin, sulphonilureas, fibrats, dexfenfluramine, troglitazone, doxazosin, ACE-inhibitors.
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pubmed:language |
ita
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0391-1977
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
37-52
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9844354-Diabetes Mellitus, Type 2,
pubmed-meshheading:9844354-Dose-Response Relationship, Drug,
pubmed-meshheading:9844354-Enzyme Activation,
pubmed-meshheading:9844354-Humans,
pubmed-meshheading:9844354-Hyperglycemia,
pubmed-meshheading:9844354-Hypoglycemic Agents,
pubmed-meshheading:9844354-Insulin,
pubmed-meshheading:9844354-Insulin Resistance,
pubmed-meshheading:9844354-Muscle, Skeletal,
pubmed-meshheading:9844354-Mutation,
pubmed-meshheading:9844354-Obesity,
pubmed-meshheading:9844354-Phosphorylation,
pubmed-meshheading:9844354-Receptor, Insulin,
pubmed-meshheading:9844354-Signal Transduction
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pubmed:year |
1998
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pubmed:articleTitle |
[Insulin resistance. Receptor and post-receptor abnormalities].
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pubmed:affiliation |
Servizio di Dietologia e Diabetologia, Ospedale Forlanini, Roma.
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pubmed:publicationType |
Journal Article,
English Abstract,
Review
|