pubmed-article:2058663 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C0080103 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C0205054 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C0001026 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1418818 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1441547 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1264633 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1151633 | lld:lifeskim |
pubmed-article:2058663 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:2058663 | pubmed:issue | 6 Pt 1 | lld:pubmed |
pubmed-article:2058663 | pubmed:dateCreated | 1991-7-30 | lld:pubmed |
pubmed-article:2058663 | pubmed:abstractText | We measured the contribution of glucose to hepatic cytosolic acetyl-CoA in vivo in rats and compared it with the phosphorylation state of a potentially regulatory enzyme complex [pyruvate dehydrogenase (PDH)]. Xenobiotic probes were used to sample hepatic cytosolic acetyl-CoA [acetylated sulfamethoxazole (SMX)] and UDP-glucose (glucuronidated acetaminophen) in vivo during [U-14C]glucose infusions. Percent active (dephosphorylated) form of PDH (PDHa) was determined on freeze-clamped liver. First, we confirmed using liver cell elutriation that acetylation of SMX occurs in parenchymal hepatocytes. Next, the fraction of cytosolic acetyl-CoA derived from [14C]glucose in vivo was shown to depend on dietary state. Specific activity of acetyl-CoA relative to plasma glucose or hepatic UDP-glucose was lower after 48 h fasting than after overnight fasting, and glucose refeeding (25 mg.kg-1.min-1 iv) maximally increased [14C]-glucose fractional contribution to acetyl-CoA within 2 h in the overnight-fasted but not in the prolonged fasted group. Hepatic PDHa demonstrated a similar but not identical pattern. The isotopic and enzymatic parameters showed significant correlations (r2 = 0.61 in 48-h fasted-refed group, r2 = 0.28 in overnight-fasted refed group), although [14C]glucose contribution to acetyl-CoA increased disproportionately compared with PDHa as refeeding progressed. The indirect pathway of UDP-glucose synthesis correlated inversely with the fractional contribution of glucose to acetyl-CoA. In summary, the fraction of hepatic acetyl-CoA derived from glucose in vivo is influenced by acute and chronic dietary factors and is only partially explained by PDHa. Regulation of the carbon source of hepatic acetyl-CoA in vivo and interactions suggested by these results (e.g., glucose-fatty acid cycle; branch-point regulation of glucose recycling) can be addressed in a quantitative fashion using this experimental framework. | lld:pubmed |
pubmed-article:2058663 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2058663 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2058663 | pubmed:language | eng | lld:pubmed |
pubmed-article:2058663 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2058663 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2058663 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2058663 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2058663 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2058663 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2058663 | pubmed:month | Jun | lld:pubmed |
pubmed-article:2058663 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:WuKK | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:HellersteinM... | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:CesarDD | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:KaempferSS | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:BlackhamMM | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:ChristiansenM... | lld:pubmed |
pubmed-article:2058663 | pubmed:author | pubmed-author:XuanZ RZR | lld:pubmed |
pubmed-article:2058663 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2058663 | pubmed:volume | 260 | lld:pubmed |
pubmed-article:2058663 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2058663 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2058663 | pubmed:pagination | E865-75 | lld:pubmed |
pubmed-article:2058663 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:2058663 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:2058663 | pubmed:articleTitle | Fraction of hepatic cytosolic acetyl-CoA derived from glucose in vivo: relation to PDH phosphorylation state. | lld:pubmed |
pubmed-article:2058663 | pubmed:affiliation | Department of Nutritional Sciences, University of California, Berkeley 94720. | lld:pubmed |
pubmed-article:2058663 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2058663 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2058663 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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