The role of ?diabetogenic? hormones on carbohydrate and lipid metabolism following oral glucose loading in insulin dependent diabetics: Effects of acute hormone administration
Open Access
- 1 October 1981
- journal article
- research article
- Published by Springer Nature in Diabetologia
- Vol. 21 (4) , 387-393
- https://doi.org/10.1007/bf00252687
Abstract
To evaluate the relative role of “diabetogenic” hormones as insulin antagonists in severe derangements of diabetic control, glucagon, cortisol, growth hormone and adrenaline were administered by continuous intravenous infusion, separately and in combination, to ketosis-prone insulin-dependent diabetics (n=11). The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Raising plasma hormone concentrations acutely into the range seen in severe diabetic states (glucagon 517±70 pg/ml; cortisol 32±3 μg/dl; growth hormone 14±3 ng/ml) did not alter significantly blood glucose profile and insulin requirement (control 11.3±1.1 U; glucagon 11.6±2.0 U; cortisol 11.1±0.4 U; growth hormone 12.9±1.4U), except for adrenaline (plasma level 550±192 pg/ml), which caused a marked rise in blood glucose levels and a threefold increase in insulin demand (31.1±3.7 U). Combined infusion of all hormones did not potentiate significantly the latter effect (38.3±4.7 U). The effectiveness of metabolic control by insulin was assessed by a marked decrease in plasma non-esterified free fatty acids and ketone bodies upon its administration after glucose ingestion in all groups studied. It is concluded that from the hormones investigated within this study adrenaline exerts the strongest diabetogenic action during its short term administration followed by that of growth hormone. Whereas it may well be that over-insulinization of the patients by the glucose controlled insulin infusion system has overcome and disguised the smaller diabetogenic effects of cortisol and glucagon.Keywords
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