Publications by authors named "Tronier B"

In 14 patients with acute pancreatitis during 16 episodes of the disease the concentrations of blood glucose, serum insulin (IRI), C-peptide (CP), and proinsulin (Pro) were determined in the fasting state on d 1, 2, 3, 5, and 10 after the attack. The peptides were measured using RIAs, and for determination of CP two antibodies: Byk-Mallinckrodt's and more specific M-1221 Novo antibodies were used. Apart from sporadic rises in the initial period of the disease, the blood glucose level did not change significantly and had a decreasing trend.

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14 patients with acute pancreatitis during 16 episodes of the disease were studied. The concentration was measured of blood glucose, serum insulin (IRI), serum C-peptide (CP) using two methods: with Byk-Mallinckrodt kits and with more specific M-1221 antibodies Novo, and of serum proinsulin (Pro) in fasting state on days 1, 2, 3, 5 and 10 after the acute onset. Apart from some sporadic rises in the initial period of the disease, the blood glucose level did not change significantly, and had rather a decreasing trend.

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beta-Cell function and glucose metabolism were studied in eight insulin-dependent diabetic recipients of combined segmental pancreas and kidney transplant with peripheral insulin delivery (Px), in eight nondiabetic kidney-transplant individuals (Kx), and in eight normal subjects (Ns) after three consecutive mixed meals. All subjects had normal fasting plasma glucose, but increased basal levels of C-peptide were demonstrated in the transplant groups (P < 0.05 relative to Ns).

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Insulin was withdrawn from 7 patients with Type I (insulin-dependent) diabetes and 4 patients with insulin-dependent diabetes secondary to chronic pancreatitis, both groups without residual beta-cell function. Median plasma glucagon concentrations rose slightly, but significantly after withdrawal of insulin in Type I diabetic patients (from 14 (range: 11-16) to 19 (14-25) pmol/l by 6 h), but not in the patients with secondary diabetes. This was accompanied by a significantly higher increase in blood glucose concentration from 5.

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Glucose-stimulated insulin secretion is depressed by training. To further elucidate the beta-cell adaptation to training, a nonglucose secretagogue was applied. Arginine was infused for 90 min to seven trained and seven untrained young men.

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Glucose counterregulation and hormonal responses after insulin-induced hypoglycemia were investigated in six patients with diabetes mellitus secondary to chronic pancreatitis, in seven with insulin-dependent (type I) diabetes mellitus, and in seven healthy subjects. Glucose counterregulation was identical in type I patients and in the patients with chronic pancreatitis, whereas both groups had impaired glucose recovery compared with the healthy subjects. The patients with chronic pancreatitis had no glucagon response to hypoglycemia, whereas epinephrine increased significantly.

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A simple and cheap one-step enzymatic method has been developed for the determination of 1-14C-glucose in plasma. C-1 of glucose is cleaved off as CO2 by treatment with hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconic dehydrogenase. True 1-14C-glucose activity is then calculated as the difference between total radioactivity and radioactivity remaining after enzyme treatment and evaporation.

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A surgical model for catheterization at multiple sites has been developed for use in long-term metabolic studies. For blood sampling, catheters were inserted into the portal and hepatic veins and the common carotid artery. The hepatic vein catheter was inserted from the margin of a liver lobe and led through the venous system, until the tip was close to the bifurcation with the inferior vena cava.

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Pharmacological, percutaneous celiac plexus blockade is often inefficient in the treatment of pain in chronic pancreatitis. Lack of efficiency could be due to incomplete denervation of the plexus; however, a method for measuring the completeness of celiac plexus blockade is not yet available. We have, therefore, monitored the physiological completeness of pharmacological percutaneous celiac blockade with 40 ml 25% ethanol by measuring the effect of posture on heart rate, blood pressure, hepato-splanchnic vascular resistance, and pancreatic hormone concentrations before and after celiac plexus block in 6 patients with chronic pancreatitis.

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Physical training decreases glucose-stimulated insulin secretion. To further explore the influence of the level of daily physical activity on beta-cell secretion, the effect of 7 days of bed rest was studied in six young, healthy men by sequential hyperglycemic clamp technique (7, 11, and 20 mM glucose, each step lasting 90 min). At 11 and 20 mM glucose, insulin concentrations in plasma were higher after (87 +/- 11 and 303 +/- 63 microU/ml) than before (63 +/- 5 and 251 +/- 50 microU/ml, P less than 0.

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Unlabelled: We studied the effect of training and detraining on the dose-response relationship between plasma glucose and beta-cell secretion in seven trained young men using sequential hyperglycemic clamp technique (7, 11, and 20 mM). Experiments were performed in the habitual state 15 h after last training session (T) as well as after 5 days of detraining (DT). Results were compared to data from seven untrained subjects (UT).

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Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] were subjected to three sequential hyperinsulinemic euglycemic clamps 15 h after having performed their last training session (T).

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Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] underwent sequential hyperinsulinemic euglycemic clamps on three occasions: 1) in the "habitual state" 15 h after the last training bout (C), 2) after 60 min of bicycle exercise at 72 +/- 3% of VO2max performed in the habitual state (E), and 3) 5 days after the last ordinary training session (detrained, DT).

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Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. No significant differences were found between the two diabetic groups regarding glucagon responses to arginine and meal ingestion. In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal.

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Controversy exists over differences in hormonal counterregulatory (CR) responses to human and porcine insulins with conflicting reports regarding the adrenaline, glucagon, growth hormone, cortisol and prolactin responses to the two species of insulin. It has been suggested that these differences may represent different central nervous system sensitivities to the two types of insulin. The CR responses to an intravenous bolus of 0.

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To investigate whether exertion changes beta-cell reactivity to glucose stimulation and to characterize the beta-cell response to glucose in humans, we performed four sequential 90-min hyperglycemic clamps (7, 11, 20, and 35 mM). Concentrations of hormones and metabolites involved in glucoregulation were measured. Metabolic rate and substrate utilization were studied by indirect calorimetry.

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The effect of acute physical exercise on insulin sensitivity and responsiveness of glucose uptake and hepatic glucose production was studied. Seven untrained men were subjected to four sequential euglycemic hyperinsulinemic clamps after rest (R), immediately after exercise (E), as well as 48 h after 60 min of 150 W ergometer exercise (ER). Insulin-mediated glucose uptake was higher on E and ER days compared with R days.

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Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .

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Norepinephrine-induced vasoconstriction, which is mediated by alpha-adrenergic receptors, is accentuated in patients with autonomic neuropathy. In contrast, responses mediated by beta-adrenergic receptors, including vasodilatation and metabolic changes, have not been evaluated in these patients. To study these responses, we administered epinephrine in a graded intravenous infusion (0.

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Plasma concentrations of insulin, C-peptide, and proinsulin were measured in different vascular beds in order to determine renal, hepatic, and systemic kinetics of the endogenous peptides in the fasting condition. Nineteen nondiabetic subjects were studied, two were normal, nine had minor vascular disorders, four had cirrhosis without organic kidney disease, and four had organic kidney disease with moderately decreased glomerular filtration rate. In subjects without organic kidney disease the arteriorenal venous extraction ratios of insulin, C-peptide, and proinsulin were mean 0.

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Glucose, 25 g, was infused iv with or without sham-feeding in seven normal males. Sham-feeding improved glucose tolerance, incremental area of blood glucose being 63% (P less than 0.05) of that during iv glucose without sham-feeding.

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In a 3 yr epidemiological cohort study of 273 diabetics treated with oral hypoglycaemic agents (OHA) and 60 diet-treated diabetics the predictive value of fasting plasma C-peptide levels was assessed with the attempt to discriminate between insulin dependence and non-insulin dependence. Serum insulin, blood glucose, haemoglobin AI, bicarbonate, urine for ketone bodies, height and weight were measured too. All but 8 OHA-treated patients (97%) had fasting C-peptide greater than 0.

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