pubmed-article:1826300 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C0030362 | lld:lifeskim |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C0007613 | lld:lifeskim |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
pubmed-article:1826300 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:1826300 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:1826300 | pubmed:dateCreated | 1991-5-7 | lld:pubmed |
pubmed-article:1826300 | pubmed:abstractText | To study the interaction between insulin secretion and insulin action in maintaining glucose homeostasis, we induced experimental insulin resistance in eight normal baboons, in six baboons treated with 40 mg/kg streptozocin (STZ-40), and in six baboons treated with 200 mg/kg streptozocin (STZ-200). Insulin resistance was induced by a 20-d continuous intravenous infusion of nicotinic acid (NA). Normal animals showed compensatory increases in several measures of insulin secretion (fasting insulin [FI], acute insulin response to arginine [AIRarg], acute insulin response to glucose [AIRgluc], and glucose potentiation slope [delta AIRarg/delta G]), with no net change in fasting plasma glucose (FPG) or glycosylated hemoglobin (HbAtc). STZ-40 animals showed compensatory increases in FI, AIRarg, and AIRgluc, but delta AIRarg/delta G failed to compensate. Although FPG remained normal in this group during NA infusion, HbA1c rose significantly. STZ-200 animals failed to show compensatory changes in both AIRgluc and delta AIRarg/delta G, with both HbA1c and FPG rising. These animals showed a paradoxical inhibition of insulin secretion in response to intravenous glucose during NA infusion, at a time when they were hyperglycemic. These data indicate that a significant degree of insulin resistance does not cause hyperglycemia in the presence of normal B cell function but, in animals with reduced B cell mass and superimposed insulin resistance, the degree of hyperglycemia is proportional to the degree of pancreatic B cell dysfunction. | lld:pubmed |
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pubmed-article:1826300 | pubmed:language | eng | lld:pubmed |
pubmed-article:1826300 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1826300 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:1826300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1826300 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1826300 | pubmed:month | Apr | lld:pubmed |
pubmed-article:1826300 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:1826300 | pubmed:author | pubmed-author:KahnS ESE | lld:pubmed |
pubmed-article:1826300 | pubmed:author | pubmed-author:KoerkerD JDJ | lld:pubmed |
pubmed-article:1826300 | pubmed:author | pubmed-author:PalmerJ PJP | lld:pubmed |
pubmed-article:1826300 | pubmed:author | pubmed-author:McCullochD... | lld:pubmed |
pubmed-article:1826300 | pubmed:author | pubmed-author:SchwartzM WMW | lld:pubmed |
pubmed-article:1826300 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1826300 | pubmed:volume | 87 | lld:pubmed |
pubmed-article:1826300 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1826300 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1826300 | pubmed:pagination | 1395-401 | lld:pubmed |
pubmed-article:1826300 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:1826300 | pubmed:meshHeading | pubmed-meshheading:1826300-... | lld:pubmed |
pubmed-article:1826300 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1826300 | pubmed:articleTitle | Effect of nicotinic acid-induced insulin resistance on pancreatic B cell function in normal and streptozocin-treated baboons. | lld:pubmed |
pubmed-article:1826300 | pubmed:affiliation | Department of Medicine, University of Washington, Seattle 98108. | lld:pubmed |
pubmed-article:1826300 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1826300 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1826300 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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