作者: Daniel H. Mintz , Joseph L. Finster , Andrew L. Taylor , Alexander Fefer
DOI: 10.1016/0002-9343(68)90037-5
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摘要: Abstract The hormonal genesis of glucose intolerance following hypoglycemia was investigated. During insulin tolerance tests, with and without pharmacologic blockade alpha receptors or cortisol production, the disposal rate orally administered found to be impaired, secretion reduced growth hormone enhanced. rebound increase in plasma free fatty acids response inhibited by oral ingestion glucose; thus elevated acid concentrations were not observed during posthypoglycemic intolerance. When an injection prevented a constant infusion, subsequent responsiveness normal, inhibited. individual contributions endogenous hypoinsulinism enhanced could readily distinguished. However, patients panhypopituitarism monotrophic deficiencies demonstrated normal insulin-induced hypoglycemia, despite impoverished response. data interpreted indicate that augmentation is major consequence which leads