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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2006-7-14
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pubmed:abstractText |
The pathophysiology of type 2 diabetes is characterized by defects in insulin action and in insulin secretion. Metabolic actions of insulin are mediated by the insulin receptor/IRS/PI 3-kinase signaling pathway in insulin's target organs including the liver, skeletal muscle and adipose tissue. Recent evidence suggests that insulin action in the brain also plays an important role in the regulation of glucose metabolism in the liver. Insulin signaling in pancreatic beta cells appears to regulate glucose-induced insulin secretion. Although the mechanism how insulin resistance develops is not fully understood, dysregulation of fatty acid metabolism, abnormalities of the function and the secretion of adipokines, as well as the increase in stress signaling might contribute to the development of insulin resistance.
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pubmed:language |
jpn
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/INSR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRS1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0047-1852
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
64
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1381-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16838661-Adipocytes,
pubmed-meshheading:16838661-Adiponectin,
pubmed-meshheading:16838661-Antigens, CD,
pubmed-meshheading:16838661-Brain,
pubmed-meshheading:16838661-Cell Division,
pubmed-meshheading:16838661-Diabetes Mellitus, Type 2,
pubmed-meshheading:16838661-Dyslipidemias,
pubmed-meshheading:16838661-Glucose,
pubmed-meshheading:16838661-Humans,
pubmed-meshheading:16838661-Insulin,
pubmed-meshheading:16838661-Insulin Receptor Substrate Proteins,
pubmed-meshheading:16838661-Insulin Resistance,
pubmed-meshheading:16838661-Insulin-Secreting Cells,
pubmed-meshheading:16838661-Liver,
pubmed-meshheading:16838661-Muscle, Skeletal,
pubmed-meshheading:16838661-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:16838661-Phosphoproteins,
pubmed-meshheading:16838661-Receptor, Insulin,
pubmed-meshheading:16838661-Signal Transduction
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pubmed:year |
2006
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pubmed:articleTitle |
[Insulin signaling and pathophysiology of type 2 diabetes mellitus].
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pubmed:affiliation |
Department of Clinical Molecular Medicine, Division of Diabetes, Digestive and Kidney Diseases, Kobe University Graduate School of Medicine.
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pubmed:publicationType |
Journal Article,
English Abstract,
Review
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