Source:http://linkedlifedata.com/resource/pubmed/id/16186400
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
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| pubmed:dateCreated |
2005-9-27
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| pubmed:abstractText |
Although hyperhomocysteinemia, an independent cardiovascular risk factor, is common in type 2 diabetes with nephropathy, the mechanism(s) of this alteration is not known. In healthy humans, hyperinsulinemia increases methionine transmethylation, homocysteine transsulfuration, and clearance. No such data exist in type 2 diabetes either in the fasting state or in response to hyperinsulinemia. To this purpose, seven male type 2 diabetic patients with albuminuria (1.2 +/- 0.4 g/day, three with mild to moderate renal insufficiency) and seven matched control subjects were infused for 6 h with L-[methyl-(2)H(3), 1-(13)C]methionine. Methionine flux, transmethylation, and disposal into proteins as well as homocysteine remethylation, transsulfuration, and clearance were determined before and after euglycemic hyperinsulinemia (approximately 1,000 pmol/l). In type 2 diabetic subjects, homocysteine concentration was twofold greater (P < 0.01) and methionine transmethylation and homocysteine clearance lower (from approximately 15 to >50% and from approximately 40 to >100%, respectively; P < 0.05) than in control subjects. The insulin-induced increments of methionine transmethylation, homocysteine transsulfuration, and clearance were markedly reduced in type 2 diabetic subjects (by more than threefold, P < 0.05 or less vs. control subjects). In contrast, methionine methyl and carbon flux were not increased in the patients. In conclusion, pathways of homocysteine disposal are impaired in type 2 diabetes with nephropathy, both in postabsorptive and insulin-stimulated states, possibly accounting for the hyperhomocysteinemia of this condition.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Dioxide,
http://linkedlifedata.com/resource/pubmed/chemical/Hemoglobin A, Glycosylated,
http://linkedlifedata.com/resource/pubmed/chemical/Homocysteine,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Methionine,
http://linkedlifedata.com/resource/pubmed/chemical/Methylenetetrahydrofolate...,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfur
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0012-1797
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
54
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2968-76
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:16186400-Blood Glucose,
pubmed-meshheading:16186400-Carbon Dioxide,
pubmed-meshheading:16186400-Diabetes Mellitus, Type 2,
pubmed-meshheading:16186400-Diabetic Nephropathies,
pubmed-meshheading:16186400-Fasting,
pubmed-meshheading:16186400-Food,
pubmed-meshheading:16186400-Glucose Clamp Technique,
pubmed-meshheading:16186400-Hemoglobin A, Glycosylated,
pubmed-meshheading:16186400-Heterozygote,
pubmed-meshheading:16186400-Homocysteine,
pubmed-meshheading:16186400-Homozygote,
pubmed-meshheading:16186400-Humans,
pubmed-meshheading:16186400-Insulin,
pubmed-meshheading:16186400-Kinetics,
pubmed-meshheading:16186400-Male,
pubmed-meshheading:16186400-Methionine,
pubmed-meshheading:16186400-Methylation,
pubmed-meshheading:16186400-Methylenetetrahydrofolate Reductase (NADPH2),
pubmed-meshheading:16186400-Middle Aged,
pubmed-meshheading:16186400-Mutation,
pubmed-meshheading:16186400-Sulfur
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| pubmed:year |
2005
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| pubmed:articleTitle |
Effects of insulin on methionine and homocysteine kinetics in type 2 diabetes with nephropathy.
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| pubmed:affiliation |
Department of Clinical and Experimental Medicine, University of Padova, Italy. paolo.tessari@unipd.it
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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