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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2011-5-24
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pubmed:abstractText |
Human immunodeficiency virus (HIV) infection is associated with insulin resistance. HIV type 1 Nef downregulates cell surface protein expression, alters signal transduction, and interacts with the cytoskeleton and proteins involved in actin polymerization. These functions are required for glucose uptake by insulin-stimulated adipocytes. We sought to determine whether Nef alters adipocyte glucose homeostasis. Using radiolabeled glucose, we found that adipocytes exposed to recombinant Nef took in 42% less glucose after insulin stimulation than did control cells. This reduction resulted from a Nef-dependent inhibition of glucose transporter 4 (GLUT4) trafficking, as assessed by means of immunofluorescence microscopy. Immunoblot analysis revealed a decrease in phosphorylation of signal transducing proteins after Nef treatment, and fluorescence microscopy showed a dramatic alteration in cortical actin organization. We conclude that Nef interferes with insulin-stimulated processes in adipocytes. We have identified HIV Nef, which is detectable and antigenic in serum samples from HIV-infected people, as a novel contributor to the development of insulin resistance.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/GTPase-Activating Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Tbc1d4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/nef Gene Products, Human...,
http://linkedlifedata.com/resource/pubmed/chemical/nef protein, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1537-6613
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
203
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1824-31
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21606541-3T3-L1 Cells,
pubmed-meshheading:21606541-Actins,
pubmed-meshheading:21606541-Adipocytes,
pubmed-meshheading:21606541-Animals,
pubmed-meshheading:21606541-Blotting, Western,
pubmed-meshheading:21606541-Cell Membrane,
pubmed-meshheading:21606541-Dose-Response Relationship, Drug,
pubmed-meshheading:21606541-Down-Regulation,
pubmed-meshheading:21606541-GTPase-Activating Proteins,
pubmed-meshheading:21606541-Glucose,
pubmed-meshheading:21606541-Glucose Transporter Type 4,
pubmed-meshheading:21606541-HIV Infections,
pubmed-meshheading:21606541-HIV-1,
pubmed-meshheading:21606541-Humans,
pubmed-meshheading:21606541-Insulin,
pubmed-meshheading:21606541-Insulin Resistance,
pubmed-meshheading:21606541-Mice,
pubmed-meshheading:21606541-Phosphorylation,
pubmed-meshheading:21606541-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:21606541-Signal Transduction,
pubmed-meshheading:21606541-nef Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2011
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pubmed:articleTitle |
Nef inhibits glucose uptake in adipocytes and contributes to insulin resistance in human immunodeficiency virus type I infection.
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pubmed:affiliation |
Department of Pharmacological Sciences, State University of New York at Stony Brook, NY 11794-8153, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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