pubmed-article:833277 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:833277 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:833277 | lifeskim:mentions | umls-concept:C0037659 | lld:lifeskim |
pubmed-article:833277 | lifeskim:mentions | umls-concept:C0596620 | lld:lifeskim |
pubmed-article:833277 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:833277 | pubmed:dateCreated | 1977-3-15 | lld:pubmed |
pubmed-article:833277 | pubmed:abstractText | Cyclic somatostatin was administered intravenously (10 mug/min for 60 min) to 10 healthy overnight fasted (postabsorptive) subjects and to 5 healthy 60-h fasted subjects. In both groups, arterial insulin and glucagon fell 50% and splanchnic release of these hormones was inhibited. In the overnight fasted subjects splanchnic glucose output fell 70%, splanchnic uptake of lactate and pyruvate was unchanged, alanine uptake fell by 25%, and glycerol uptake rose more than twofold in parallel with an increase in arterial glycerol. In the 60-h fasted group splanchnic glucose output was less than 40% of that observed in the overnight fasted subjects. Somatostatin led to a further decrease (--70%) in glucose production. Splanchnic uptake of lactate and pyruvate fell by 30-40%, amino acid uptake was unchanged, while uptake of glycerol rose fivefold. Total uptake of glucose precursors thus exceeded the simultaneous glucose output by more than 200%. Splanchnic uptake of FFA rose fourfold during somatostatin while output of beta-hydroxybutyrate increased by 75%. Estimated hepatic blood flow fell 25-35% and returned to base line as soon as the somatostatin infusion ended. It is concluded that (a) somatostatin-induced hypoglucagonemia results in inhibition of splanchnic glucose output in glycogen-depleted, 60-h fasted subjects as well as in postabsorptive subjects, indicating an effect of glucagon on hepatic gluconeogenesis as well as glycogenolysis; (b) the glucagonsensitive step(s) in gluconeogenesis affected by somatostatin involves primarily intra-hepatic disposal rather than net hepatic uptake of glucose precursors; (c) splanchnic uptake of fatty acids and ketone output are increased in the face of combined insulin and glucagon deficiency; and (d) diminished splanchnic blood flow may contribute to some of the effects of somatostatin on splanchnic metabolism. | lld:pubmed |
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pubmed-article:833277 | pubmed:language | eng | lld:pubmed |
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pubmed-article:833277 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:833277 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:833277 | pubmed:month | Feb | lld:pubmed |
pubmed-article:833277 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:FeligPP | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:LuftRR | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:Efendi?SS | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:HagenfeldtLL | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:WahrenJJ | lld:pubmed |
pubmed-article:833277 | pubmed:author | pubmed-author:BjörkmanOO | lld:pubmed |
pubmed-article:833277 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:833277 | pubmed:volume | 59 | lld:pubmed |
pubmed-article:833277 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:833277 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:833277 | pubmed:pagination | 299-307 | lld:pubmed |
pubmed-article:833277 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:833277 | pubmed:year | 1977 | lld:pubmed |
pubmed-article:833277 | pubmed:articleTitle | Influence of somatostatin on splanchnic glucose metabolism in postabsorptive and 60-hour fasted humans. | lld:pubmed |
pubmed-article:833277 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:833277 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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