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Due to their reported 'glucose‐intolerant' phenotype, rainbow trout have been the focus of comparative studies probing underlying endocrine mechanisms at the organismal, tissue and molecular level. A particular focus has been placed on the investigation of the comparative role of insulin, an important glucoregulatory hormone, and its interaction with macronutrients. A limiting factor in the comparative investigation of insulin is the current lack of reliable assays to quantify circulating mature and thus bioactive insulin. To circumvent this limitation, tissue‐specific responsiveness to postprandial or exogenous insulin has been quantified at the level of post‐translational modifications of cell signalling proteins. These studies revealed that the insulin responsiveness of these proteins and their post‐translational modifications are evolutionarily highly conserved and thus provide useful and quantifiable proxy indices to investigate insulin function in rainbow trout. While the involvement of specific branches of the intracellular insulin signalling pathway (e.g., mTor) in rainbow trout glucoregulation have been successfully probed through pharmacological approaches, it would be useful to have a functionally validated insulin receptor antagonist to characterize the glucoregulatory role of the insulin receptor pathway in its entirety for this species. Here, we report two separate in vivo experiments to test the ability of the mammalian insulin receptor antagonist, S961, to efficiently block insulin signalling in liver and muscle in response to endogenously released insulin and to exogenously infused bovine insulin. We found that, irrespective of the experimental treatment or dose, activation of the insulin pathway in liver and muscle was not inhibited by S961, showing that its antagonistic effect does not extend to rainbow trout. [ABSTRACT FROM AUTHOR]

In order to clarify the inhibitory mechanism of insulin secretion associated with open-heart surgery, the influence of insulin antagonistic hormones on insulin secretion was studied in 20 patients with congenital heart diseases undergoing open-heart surgery, under simple deep hypothermia. Despite a hyperglycemia, plasma immunoreactive insulin and C-peptide showed no change during the cooling period, while with the exception of plasma human growth hormone, dopamine-β-hydroxylase, immunoreactive glucagon, cortisol and cyclic AMP in plasma, either showed no change, or a decrease during the cooling period. It is assumed that catecholamine, glucocorticoid and glucagon do not play an important role in the inhibitory mechanism of insulin secretion during hypothermic open-heart surgery, and a transient hypofunction of the pancreas as well as the liver and the adrenal gland is probably involved. [ABSTRACT FROM AUTHOR]

Nine patients were studied 1.5-3 years after jejuno-ileostomy for obesity by an intravenous glucose infusion technique designed to imitate blood glucose concentrations after glucose ingestion. Whereas serum insulin and gastrin concentrations were normal, blood glucose concentrations were significantly depressed compared to preoperative levels as well as to levels in matched normal subjects. Thus, in the fasting state mean concentrations (± S.E.M.) of blood glucose, serum insulin and gastrin in the patients were, respectively, 3.3±0.2 mmol/l, 95±22 pmol/l and 38±4 pmol/l. The corresponding concentrations in the matched normals were 4.3±0.2 mmol/l, 70±18 pmol/l and 39±6 pmol/l. The glucose concentrations in the patients were low in all situations, i. e. in the fasting state, after oral glucose ingestion and during the intravenous glucose infusion. The results indicate that jejuno-ileostomy in obesity greatly facilitates peripheral glucose disposal. The mechanism behind this phenomenon is not yet known. [ABSTRACT FROM AUTHOR]