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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
1990-12-4
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pubmed:abstractText |
To assess the role of muscle and liver in the pathogenesis of postprandial hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM), we administered an oral glucose load enriched with [14C]glucose to 10 NIDDM subjects and 10 age- and weight-matched nondiabetic volunteers and compared muscle glucose disposal by measuring forearm balance of glucose, lactate, alanine, O2, and CO2 (with forearm calorimetry). In addition, we used the dual-lable isotope method to compare overall rates of glucose appearance (Ra) and disappearance (Rd), suppression of endogenous glucose output, and splanchnic glucose sequestration. During the initial 1-1.5 h after glucose ingestion, plasma glucose increased by approximately 8 mM in NIDDM vs. approximately 3 mM in nondiabetic subjects (P less than 0.01); overall glucose Ra was nearly 11 g greater in NIDDM than nondiabetic subjects (45.1 +/- 2.3 vs. 34.4 +/- 1.5 g, P less than 0.01), but glucose Rd was not significantly different in NIDDM (35.1 +/- 2.4 g) and nondiabetic (33.3 +/- 2.7 g) subjects. The greater overall glucose Ra of NIDDM subjects was due to 6.8 g greater endogenous glucose output (13.7 +/- 1.1 vs. 6.8 +/- 1.0 g, P less than 0.01) and 3.8 g less oral glucose splanchnic sequestration of the oral load (31.4 +/- 1.5 vs. 27.5 +/- 0.9 g, P less than 0.05). Although glucose taken up by muscle was not significantly different in NIDDM and nondiabetic subjects (39.3 +/- 3.5 vs. 41.0 +/- 2.5 g/5 h), a greater amount of the glucose taken up by muscle in NIDDM was released as lactate and alanine (11.7 +/- 1.0 vs. 5.2 +/- 0.3 g in nondiabetic subjects, P less than 0.01), and less was stored (11.7 +/- 1.3 vs. 16.9 +/- 1.5 g, P less than 0.05). We conclude that increased systemic glucose delivery, due primarily to reduced suppression of endogenous hepatic glucose output and, to a lesser extent, reduced splanchnic glucose sequestration, is the predominant factor responsible for postprandial hyperglycemia in NIDDM.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alanine,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Dioxide,
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Radioisotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Lactates,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0012-1797
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1381-90
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2121568-Administration, Oral,
pubmed-meshheading:2121568-Alanine,
pubmed-meshheading:2121568-Blood Glucose,
pubmed-meshheading:2121568-Carbon Dioxide,
pubmed-meshheading:2121568-Carbon Radioisotopes,
pubmed-meshheading:2121568-Diabetes Mellitus, Type 2,
pubmed-meshheading:2121568-Female,
pubmed-meshheading:2121568-Glucose,
pubmed-meshheading:2121568-Humans,
pubmed-meshheading:2121568-Hyperglycemia,
pubmed-meshheading:2121568-Insulin,
pubmed-meshheading:2121568-Lactates,
pubmed-meshheading:2121568-Liver,
pubmed-meshheading:2121568-Male,
pubmed-meshheading:2121568-Middle Aged,
pubmed-meshheading:2121568-Muscles,
pubmed-meshheading:2121568-Oxygen,
pubmed-meshheading:2121568-Time Factors
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pubmed:year |
1990
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pubmed:articleTitle |
Contribution of abnormal muscle and liver glucose metabolism to postprandial hyperglycemia in NIDDM.
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pubmed:affiliation |
Department of Medicine, University of Pittsburgh School of Medicine, PA.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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