Source:http://linkedlifedata.com/resource/pubmed/id/12006367
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2002-5-13
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| pubmed:abstractText |
The effects of insulin-like growth factor I (IGF-I) and insulin on free fatty acid (FFA) and glucose metabolism were compared in eight control and eight type 2 diabetic subjects, who received a two-step euglycemic hyperinsulinemic (0.25 and 0.5 mU x kg(-1) x min(-1)) clamp and a two-step euglycemic IGF-I (26 and 52 pmol x kg(-1) x min(-1)) clamp with [3-(3)H]glucose, [1-(14)C]palmitate, and indirect calorimetry. The insulin and IGF-I infusion rates were chosen to augment glucose disposal (R(d)) to a similar extent in control subjects. In type 2 diabetic subjects, stimulation of R(d) (second clamp step) in response to both insulin and IGF-I was reduced by approximately 40-50% compared with control subjects. In control subjects, insulin was more effective than IGF-I in suppressing endogenous glucose production (EGP) during both clamp steps. In type 2 diabetic subjects, insulin-mediated suppression of EGP was impaired, whereas EGP suppression by IGF-I was similar to that of controls. In both control and diabetic subjects, IGF-I-mediated suppression of plasma FFA concentration and inhibition of FFA turnover were markedly impaired compared with insulin (P < 0.01-0.001). During the second IGF-I clamp step, suppression of plasma FFA concentration and FFA turnover was impaired in diabetic vs. control subjects (P < 0.05-0.01). CONCLUSIONS: 1) IGF-I is less effective than insulin in suppressing EGP and FFA turnover; 2) insulin-resistant type 2 diabetic subjects also exhibit IGF-I resistance in skeletal muscle. However, suppression of EGP by IGF-I is not impaired in diabetic individuals, indicating normal hepatic sensitivity to IGF-I.
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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/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0193-1849
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| pubmed:author |
pubmed-author:BajajMandeepM,
pubmed-author:BelfortRenataR,
pubmed-author:BerriaRacheleR,
pubmed-author:CusiKennethK,
pubmed-author:DeFronzoRalph ARA,
pubmed-author:KashyapSangetaS,
pubmed-author:MandarinoLawrenceL,
pubmed-author:PratipanawatrThongchaiT,
pubmed-author:PratipanawatrWilailakW,
pubmed-author:RosenCliffordC
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| pubmed:issnType |
Print
|
| pubmed:volume |
282
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
E1360-8
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:12006367-Adult,
pubmed-meshheading:12006367-Biological Transport,
pubmed-meshheading:12006367-Blood Glucose,
pubmed-meshheading:12006367-Calorimetry, Indirect,
pubmed-meshheading:12006367-Diabetes Mellitus, Type 2,
pubmed-meshheading:12006367-Drug Resistance,
pubmed-meshheading:12006367-Fatty Acids, Nonesterified,
pubmed-meshheading:12006367-Female,
pubmed-meshheading:12006367-Glucose,
pubmed-meshheading:12006367-Glucose Clamp Technique,
pubmed-meshheading:12006367-Humans,
pubmed-meshheading:12006367-Insulin,
pubmed-meshheading:12006367-Insulin Resistance,
pubmed-meshheading:12006367-Insulin-Like Growth Factor Binding Protein 3,
pubmed-meshheading:12006367-Insulin-Like Growth Factor I,
pubmed-meshheading:12006367-Lipid Peroxidation,
pubmed-meshheading:12006367-Male,
pubmed-meshheading:12006367-Middle Aged,
pubmed-meshheading:12006367-Oxidation-Reduction,
pubmed-meshheading:12006367-Tritium
|
| pubmed:year |
2002
|
| pubmed:articleTitle |
Effect of IGF-I on FFA and glucose metabolism in control and type 2 diabetic subjects.
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| pubmed:affiliation |
Diabetes Division, Department of Medicine, University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|