| pubmed-article:9151794 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C2349001 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0681850 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C1706203 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C2697811 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0026845 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0221099 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C1550501 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0596620 | lld:lifeskim |
| pubmed-article:9151794 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:9151794 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:9151794 | pubmed:dateCreated | 1997-6-24 | lld:pubmed |
| pubmed-article:9151794 | pubmed:abstractText | To determine the mechanism of impaired insulin-stimulated muscle glycogen metabolism in patients with poorly controlled insulin-dependent diabetes mellitus (IDDM), we used 13C-NMR spectroscopy to monitor the peak intensity of the C1 resonance of the glucosyl units in muscle glycogen during a 6-h hyperglycemic-hyperinsulinemic clamp using [1-(13)C]glucose-enriched infusate followed by nonenriched glucose. Under similar steady state (t = 3-6 h) plasma glucose (approximately 9.0 mM) and insulin concentrations (approximately 400 pM), nonoxidative glucose metabolism was significantly less in the IDDM subjects compared with age-weight-matched control subjects (37+/-6 vs. 73+/-11 micromol/kg of body wt per minute, P < 0.05), which could be attributed to an approximately 45% reduction in the net rate of muscle glycogen synthesis in the IDDM subjects compared with the control subjects (108+/-16 vs. 195+/-6 micromol/liter of muscle per minute, P < 0.001). Muscle glycogen turnover in the IDDM subjects was significantly less than that of the controls (16+/-4 vs. 33+/-5%, P < 0.05), indicating that a marked reduction in flux through glycogen synthase was responsible for the reduced rate of net glycogen synthesis in the IDDM subjects. 31P-NMR spectroscopy was used to determine the intramuscular concentration of glucose-6-phosphate (G-6-P) under the same hyperglycemic-hyperinsulinemic conditions. Basal G-6-P concentration was similar between the two groups (approximately 0.10 mmol/kg of muscle) but the increment in G-6-P concentration in response to the glucose-insulin infusion was approximately 50% less in the IDDM subjects compared with the control subjects (0.07+/-0.02 vs. 0.13+/-0.02 mmol/kg of muscle, P < 0.05). When nonoxidative glucose metabolic rates in the control subjects were matched to the IDDM subjects, the increment in the G-6-P concentration (0.06+/-0.02 mmol/kg of muscle) was no different than that in the IDDM subjects. Together, these data indicate that defective glucose transport/phosphorylation is the major factor responsible for the lower rate of muscle glycogen synthesis in the poorly controlled insulin-dependent diabetic subjects. | lld:pubmed |
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| pubmed-article:9151794 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9151794 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151794 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9151794 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9151794 | pubmed:month | May | lld:pubmed |
| pubmed-article:9151794 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:LaurentDD | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:MagnussonII | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:PetersenK FKF | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:ShulmanG IGI | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:RothmanD LDL | lld:pubmed |
| pubmed-article:9151794 | pubmed:author | pubmed-author:ClineG WGW | lld:pubmed |
| pubmed-article:9151794 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9151794 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9151794 | pubmed:volume | 99 | lld:pubmed |
| pubmed-article:9151794 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9151794 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9151794 | pubmed:pagination | 2219-24 | lld:pubmed |
| pubmed-article:9151794 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9151794 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9151794 | pubmed:articleTitle | Mechanism of impaired insulin-stimulated muscle glucose metabolism in subjects with insulin-dependent diabetes mellitus. | lld:pubmed |
| pubmed-article:9151794 | pubmed:affiliation | Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. | lld:pubmed |
| pubmed-article:9151794 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9151794 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9151794 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9151794 | lld:pubmed |
