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S. Efendić, A. Claro and R. Luft

ABSTRACT

In man, 3 μg per kg per 90 min of linear somatostatin significantly inhibited basal as well as arginine induced insulin and glucagon release. One μg per kg per 90 min of somatostatin significantly inhibited basal insulin release but not basal glucagon release or arginine induced insulin and glucagon release.

In the perfused rat pancreas, as little as one ng per ml of perfusate of somatostatin significantly inhibited arginine induced insulin but not glucagon release, while 10 ng per ml of somatostatin by more than 50 per cent reduced the effect of arginine on insulin and glucagon release. Thus, linear somatostatin seemed to be a slightly more potent inhibitor of insulin than of glucagon release in man and in the perfused rat pancreas.

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N. Møller, J. O. L. Jørgensen, J. Møller, L. Ørskov, N. Pørksen, K. G. M. M. Alberti and O. Schmitz

Abstract.

There is evidence that hyperketonemia in insulin-dependent diabetes may be aggravated by a decreased disposal rate for ketone bodies. To test the hypothesis that this decrease may be induced by concomitant hyperglycemia through substrate competition at the acetyl-CoA level, 5 young insulin-dependent diabetic subjects received at 2-h iv infusion of 0.9 mmol 3-hydroxybutyrate · kg−1 · h−1 at clamped 1. euglycemia (5 mmol/l) and 2. hyperglycemia (11 mmol/l) on separate occasions. To ensure similar metabolic conditions, a low-dose hyperinsulinemic euglycemic clamp was performed during the 5 h preceding the actual studies. Substrate fluxes in muscle were assessed through the forearm technique. The glucose infusion rate was 4.9 and 2.9 mg· kg−1·min−1, and the forearm arteriovenous difference for glucose was 0.72 during hyperglycemia and 0.39 mmol/l (p<0.05). during euglycemia. Hyperglycemia did not affect circulating levels of free insulin, glucagon, nonesterified fatty acids, 3-hydroxybutyrate (hyperglycemia: 665, euglycemia: 770 μmol/l, p>0.05) or acetoacetate, nor forearm uptake of 3-hydroxybutyrat (hyperglycemia, 152, euglycemia: 168 μmol/l, p>0.05). In conclusion, our results do not suggest any inhibitory role for hyperglycemia in the disposal of ketone bodies. In as much as extrapolation from the present well insulinized state is appropriate, the data indicate that alternative mechanisms may be involved in the observed impairment of ketone body clearance in hyperketonemic insulin-dependent diabetic patients.

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Panagiotis Anagnostis, Azeem Majeed, Desmond G Johnston and Ian F Godsland

The relative risk for cardiovascular disease (CVD) events and mortality in diabetic women (in comparison with non-diabetic women) is believed to be greater than that in diabetic men. However, the absolute risk for CVD mortality and morbidity does not appear to be higher in women. In general, there is heterogeneity between studies, and whether there is any definite difference in the CVD risk between sexes at any level of glycaemia is not known. The same arguments also apply when comparing the CVD risk factors, such as lipid profiles and systemic inflammation indices, which seem to be worse in women than in men with diabetes mellitus (DM). The same questions emerge at any given glycaemic state: are women at worse risk and do they have a worse risk factor profile than men? These issues have yet to be resolved. Similar, though less extensive, data have been reported for prediabetes. Furthermore, women with DM are suboptimally treated compared with men regarding lipid and blood pressure targets. Large prospective studies representative of the general population are therefore needed to define the differences between sexes regarding CVD events and mortality at a given glucose level and after adjusting for any other confounders.

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K. Gréen, O. Vesterqvist and V. Grill

Abstract. The in vivo synthesis of thromboxane A2 and prostacyclin was estimated in 23 diabetics through measurements of the major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-PGF utilizing gas chromatography-mass spectrometry. Mean excretion was similar to that in non-diabetic subjects. The possible influence of hyperglycemia on the excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-PGF was evaluated in three ways: by measuring excretion before and during an acute 9-h normalization of hyperglycemia through an artificial pancreas (Biostator) as well as by comparing excretion before and 7–12 days or 40–180 days after the initiation of insulin treatment. Despite significant reducing effects on hyperglycemia or on levels of hemoglobin A1c, no effects on the excretion of the thromboxane and prostacyclin metabolites could be found. Abnormal formation of thromboxane or prostacyclin is not a generalized feature of the diabetic state.

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Sven Karlsson and Bo Ahrén

Abstract. Besides in the brain, corticotropin-releasing hormone occurs in the pancreas. Therefore, its effects on plasma levels of insulin and glucagon were investigated in vivo in the mouse. At 2 min after CRH injection (0.5–8.0 nmol/kg), plasma insulin was lowered: by 4.0 nmol/kg from 38 ± 4 to 28 ± 2 mU/l (P < 0.05). Plasma insulin was lowered also at 6 min, whereas at 10 min, plasma insulin levels were elevated (P < 0.05). Plasma glucagon levels were slightly lowered (P < 0.05) at 10 min after CRH injection, whereas plasma glucose was slightly elevated (P < 0.05) at 6 min after injection but not at 2 or 10 min. The effects of CRH on the plasma insulin and glucagon response to iv injections of half-maximal dose levels of glucose (2.8 mmol/kg) or the cholinergic agonist carbachol (0.16 μmol/kg) were also investigated. CRH, 4.0 nmol/kg, however, could not influence the plasma insulin or glucagon levels after the iv injection of either glucose or carbachol. Thus, CRH slightly affects basal plasma levels of insulin and glucagon in mice. In contrast, stimulated insulin and glucagon secretions are not affected by CRH. Peripheral CRH may therefore be of slight importance for the regulation of basal plasma levels of insulin and glucagon in the mouse.

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F. Laurent, H. Karmann, R. Gross, M. T. Strosser and P. Mialhe

Abstract. Glucagon, somatostatin and insulin secretions were evaluated in a new type of perfusion preparation: the naturally A and D cell rich splenic bulb of duck pancreas. Stable basal levels were observed with 11 mm glucose, corresponding to normoglycaemia, and all secretions were stimulated by 1 mm 3-isobutyl-1-methyl xanthine and by 10 mm arginine, demonstrating the technique's validity. In the absence of aminoacids in the perfusion medium, A cell blindness to glucose was corrected by physiological levels of insulin (2 ng/ml); insulinodependency of A cells, and unresponsiveness of D cells to glucose, probably not ruled by insulin, were observed. However, in the presence of aminoacids, glucagon was inhibited and somatostatin secretion stimulated by glucose (33 mm), independently of insulin (2 ng/ml). Aminoacids greatly influenced pancreatic hormone release.

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Leonora S. Levine, P. G. Wright and Fanny Marcus

Abstract.

Rats fed a 6% protein diet for 14 weeks showed a normal glucose tolerance but failed to release immunoreactive insulin (IRI), following iv glucose. Furthermore the isolated perfused pancreas of the rats fed the 6% protein diet secreted eleven times less IRI than the isolated pancreas prepared from the rats reared on an 18% protein diet when both were subjected to the same glucose challenge. This difference occurred despite the fact that the total IRI content of the pancreas' was not significantly different between the two groups. In the protein-malnourished rats it is suggested that the normal glucose tolerance response, despite the failure to release a concommitant amount of IRI, may indicate increased sensitivity to IRI or may be due to the secretion in these animals of a biologically active insulin, which shows no immunological cross-reactivity with pancreatic insulin. Alternately there may be increased peripheral glucose utilisation in the low protein rats.

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Sebastiano Grasso, Giuseppe Palumbo, Franco Fallucca, Salvatore Lanzafame, Barbara Indelicato and Silvana Sanfilippo

Abstract. The development of the human endocrine pancreas is described. The hormone content and islet responsiveness of foetal and neonatal pancreases of diabetic and non-diabetic pregnant women are reported.

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Janusz Krassowski, Jean Rousselle, Evelyne Maeder and Jean-Pierre Felber

Abstract.

Ornithine-α-ketoglutarate (OAK), a drug commonly used in various catabolic states, was studied for its acute effects on endocrine pancreas. A 30-min infusion of OAK (20 g/m2) induced significant increases in insulin levels (from 15 through 60 min) and in glucagon levels (from 15 through 90 min). However, OAK-induced insulin and glucagon responses were lower than after a 0.5 g/kg arginine infusion. The fluctuations of blood glucose levels were much less marked during OAK infusion than during arginine and especially the late fall was less evident.

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H. Daweke

Using the method of glucose-1-14C oxydation to 14CO2 on the rat epididymal adipose tissue, the insulin-like activities (ILA) in the serum have been compared before and after oral loading with glucose in normal subjects, in maturity-onset diabetics and in insulin-requiring diabetics. In maturity-onset diabetics mean fasting values were found to be 30% below normal while in insulin-requiring diabetics they were 85% above normal. In normal subjects there was observed, 30 minutes after glucose loading, a moderate increase in blood sugar together with an increase of ILA of 222% above the starting value; in maturity-onset diabetics the increase in ILA was only 106% while the blood sugar was markedly increased. After glucose loading in maturity-onset diabetics, the total amount of insulin detected during the period of the experiment was, on the average, only 45% of that found in normal subjects. In insulin requiring diabetics there was no increase but, on the contrary, a steady decrease of the ILA values, while the blood sugar excessively increased. In general ILA values were higher than those in maturity-onset diabetics. No difference in response was found between maturity-onset diabetics treated with diet alone and those treated with diet and oral hypoglycaemic drugs. In contrast to the absolute ILA values, the index of insulin reserve, is of value in assessing the functional capacity of the pancreas. This index decreases progressively with the severity of the disease and reaches a maximum of 54% of the normal in maturity-onset diabetics, which can satisfactorily be explained by pancreas insufficiency.

Only in some cases of insulin-requiring diabetics was an insulin reserve still detectable. The biological inactivity of the insulin circulating in the blood can be deduced from the increased ILA-values, as compared with those found in maturity-onset diabetics. Obviously some of this insulin can be released by the addition of glucose. It is likely that, in addition to pancreatic insufficiency, insulin-binding or insulin-inactivating antibodies play a part in the pathogenesis of insulin-requiring diabetes.