Source:http://linkedlifedata.com/resource/pubmed/id/15113747
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2004-7-23
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| pubmed:abstractText |
Postprandial hyperglycemia is implicated as a risk factor predisposing to vascular complications. This study was designed to assess recurrent short-term increases in glucose on markers of renal fibrogenesis. Human renal cortical fibroblasts were exposed to fluctuating short-term (2 h) increases to 15 mM d-glucose, three times a day over 72 h, on a background of 5 mM d-glucose. To determine whether observed changes were due to fluctuating osmolality, identical experiments were undertaken with cells exposed to l-glucose. Parallel experiments were performed in cells exposed to 5 mM d-glucose and constant exposure to either 15 or 7.5 mM d-glucose. Fluctuating d-glucose increased extracellular matrix, as measured by proline incorporation (P < 0.05), collagen IV (P < 0.005), and fibronectin production (P < 0.001), in association with increased tissue inhibitor of matrix metalloproteinase (MMP) (P < 0.05). Sustained exposure to 15 mM d-glucose increased fibronectin (P < 0.001), in association with increased MMP-2 (P = 0.01) and MMP-9 activity (P < 0.05), suggestive of a protective effect on collagen matrix accumulation. Transforming growth factor-beta(1) (TGF-beta(1)) mRNA was increased after short-term (90 min) exposure to 15 mM glucose (P < 0.05) and after 24-h exposure to 7.5 mM ? (P < 0.05). Normalization of TGF-beta(1) secretion occurred within 48 h of constant exposure to an elevated glucose. Fluctuating l-glucose also induced TGF-beta(1) mRNA and a profibrotic profile, however, to a lesser extent than observed with exposure to fluctuating d-glucose. The results suggest that exposure to fluctuating glucose concentrations increases renal interstitial fibrosis compared with stable elevations in d-glucose. The effects are, in part, due to the inherent osmotic changes.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type IV,
http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Proline,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/TGFB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
1931-857X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
287
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
F268-73
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| pubmed:dateRevised |
2011-4-28
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| pubmed:meshHeading |
pubmed-meshheading:15113747-Blood Glucose,
pubmed-meshheading:15113747-Cells, Cultured,
pubmed-meshheading:15113747-Collagen Type IV,
pubmed-meshheading:15113747-Dose-Response Relationship, Drug,
pubmed-meshheading:15113747-Extracellular Matrix,
pubmed-meshheading:15113747-Fibroblasts,
pubmed-meshheading:15113747-Fibronectins,
pubmed-meshheading:15113747-Fibrosis,
pubmed-meshheading:15113747-Glucose,
pubmed-meshheading:15113747-Humans,
pubmed-meshheading:15113747-Kidney,
pubmed-meshheading:15113747-Kidney Cortex,
pubmed-meshheading:15113747-Matrix Metalloproteinase 2,
pubmed-meshheading:15113747-Matrix Metalloproteinase 9,
pubmed-meshheading:15113747-Proline,
pubmed-meshheading:15113747-RNA, Messenger,
pubmed-meshheading:15113747-Time Factors,
pubmed-meshheading:15113747-Tissue Inhibitor of Metalloproteinase-1,
pubmed-meshheading:15113747-Transforming Growth Factor beta,
pubmed-meshheading:15113747-Transforming Growth Factor beta1
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| pubmed:year |
2004
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| pubmed:articleTitle |
Short-term peaks in glucose promote renal fibrogenesis independently of total glucose exposure.
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| pubmed:affiliation |
Renal Research Group, Kolling Institute, Royal North Shore Hospital, University of Sydney, St. Leonards, New South Wales, Australia.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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