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Biomedical subjects

B Tronier

Publications and source records attributed to B Tronier.

At least 55 records · Page 3Linked to original sources
PubMed1984

Relation of immunoreactive gastric inhibitory polypeptide to changes in glycaemic control and B cell function in type 1 (insulin-dependent) diabetes mellitus.

The effect of strict glycaemic control on plasma immunoreactive gastric inhibitory polypeptide (IR-GIP) concentrations and pancreatic B cell function as estimated by plasma C-peptide was evaluated in 14 Type 1 (insulin-dependent) diabetics. The effect was estimated by giving a test meal before (test 1) and after (test 2) 1 week with near normal blood glucose control (mean blood glucose 6.7 +/- 0.2 mmol/l) and again 3 weeks later (test 3) in the outpatient clinic. The glycaemic control was significantly improved at test 2 and test 3 compared with that of test 1. The IR-GIP concentrations before and after the meals were similar at all three tests and not different from those found in 21 normal controls. In 8 patients with a significant B cell response at test 1, B cell function was significantly improved both at test 2 and test 3 but no change in fasting or post-prandial IR-GIP concentrations was found and no correlation between B cell function and IR-GIP existed. We conclude that strict glycaemic control improves B cell function but does not modulate plasma IR-GIP concentrations. Factors other than GIP seem to be of greater importance in determining the magnitude of B cell function in Type 1 diabetes.

Adolescent↗
PubMed1984

Lack of negative feed-back regulation of insulin on the responses of gastric inhibitory polypeptide, insulin, glucagon and pancreatic polypeptide to a meal in insulin treated diabetics.

The effect of insulin on the secretion of immunoreactive gastric inhibitory polypeptide, insulin (as measured by C-peptide), glucagon and pancreatic polypeptide during and after a test meal was examined in seven diabetic patients treated with high insulin doses (mean 1.12 +/- 0.12 IU/kg X 24 h) before and after a reduction of the insulin dose (to 0.62 +/- 0.04 IU/kg X 24 h, p less than 0.02). While plasma insulin concentrations were significantly higher on the higher dose, no significant differences were found in the responses of immunoreactive gastric inhibitory polypeptide, C-peptide, glucagon and pancreatic polypeptide to the two meals. Blood glucose concentrations were not significantly different at the two tests. It thus seems that insulin has no direct effect on the secretion of these substances after a meal in insulin-treated diabetics.

Adult↗
PubMed1983

Plasma somatostatin increases during hypoglycaemia in insulin-dependent patients with and without B-cell function.

Responses of somatostatin-like immunoreactivity (SLI) to hypoglycaemia were investigated in seven type 1 (insulin-dependent) patients with residual B-cell function, eight patients without B-cell function, and six healthy controls. A higher basal level of SLI was found in the group with B-cell function when compared with the group without B-cell function. The basal level in the normal subjects was in between the two diabetic groups. All the diabetics had a somatostatin response to hypoglycaemia which was independent of residual B-cell function and no different from that of normal subjects.

Adolescent↗
PubMed1983

Discrepancy between plasma C-peptide and insulin response to oral and intravenous glucose.

Plasma insulin, proinsulin, and C-peptide responses to 25 g glucose orally and intravenously administered were measured in 10 healthy males. Plasma insulin response was higher during the oral load in accordance with the "incretin" concept. However, the actual amount of insulin secreted, as measured by the plasma C-peptide response, was similar during the two glucose loads. The higher plasma insulin response after oral glucose was not due to crossreactivity with proinsulin in the insulin assay. These results suggest that the higher plasma insulin response during an oral glucose load is due at least partially to a lower hepatic extraction of insulin.

Administration, Oral↗
PubMed1983

Fasting plasma somatostatin in alcoholic liver disease.

Fasting level of somatostatin-like immunoreactivity (SLI) in plasma was measured by a highly sensitive radioimmunoassay in 36 patients with alcoholic liver disease verified by histopathology (10 patients with steatosis and 26 with cirrhosis of the liver). The median value of SLI was markedly elevated in patients with steatosis of the liver as compared to normal subjects, P less than 0.01, while the median value of SLI in the cirrhotic group was even higher, P less than 0.05, as compared to the steatotic group. Correlations of SLI to se-bilirubin and p-coagulation factors 2, 7 and 10 were significant, P less than 0.001 and P less than 0.01, respectively, whereas no correlation to plasma insulin could be elicited. These results suggest that in alcoholic liver disease fasting plasma somatostatin is correlated to the degree of hepatic failure and indicate that the liver is an important site for clearance of portal vein somatostatin.

Adult↗
PubMed1982

Hormonal, metabolic and cardiovascular responses to hypoglycaemia in Type 1 (insulin-dependent) diabetes with and without residual B cell function.

Hormonal, metabolic and cardiovascular responses to insulin induced hypoglycaemia were investigated in seven Type 1 (insulin-dependent) diabetic patients with residual B cell function, eight Type 1 diabetic patients without B cell function and six healthy subjects. No differences were found between the diabetic groups regarding nadir of glucose and rate of recovery to normoglycaemia. The patients with residual B cell function had a glucagon response to hypoglycaemia which was close to that of normal subjects. In patients without B cell function, the glucagon response to hypoglycaemia was present, albeit significantly smaller than in the patients with preserved B cell function (0.025 ng/ml, range 0.007-0.042 versus 0.054 ng/ml, range 0.029-0.087). The group without B cell function had signs of an exaggerated rate of lipolysis and ketogenesis compared with the patients with B cell function and the normal subjects.

Adult↗
PubMed1982

Kidney function and size in diabetics before and during initial insulin treatment.

GFR, RPF, and kidney size were measured in nine young recently diagnosed insulin-dependent diabetics before (days 0) and 3 and 8 days after the beginning of the initial insulin treatment and in comparable control subjects. Kidney function was measured by a constant infusion technique using I-125-iothalamate and 131-I-hippuran. Kidney size was determined by means of ultrasound. Before insulin treatment elevated values for GFR (+44%, P less than 0.01), RPF (+18%, P less than 0.05), and kidney size (+29%, P less than 0.01) were found. Near-normal metabolic control was achieved in all patients using either multiple subcutaneous injections of insulin or an artificial betacell. GFR decreased from 160 +/- 9 SEM to 141 +/- 6 ml/min X 1.73 m2 (P less than 0.01) and further to 133 +/- 5 ml/min X 1.73 m2 (P less than 0.01, compared to day 0). Renal plasma flow was 601 +/- 33 and 588 +/- 44 ml x 1.73 m2 at days 0 and 3, respectively (NS) and decreased to 558 +/- 35 ml/min x 1.73 m2 at day 0 (P less than 0.01). By contrast no statistically significant changes in kidney volume were observed; the results on day 0, 3 and 8 were 145 +/- 7, 162 +/- 11 and 143 +/- 9 ml/1.73 m2, respectively. The present study demonstrates that kidney size and function are elevated at the onset of insulin-dependent diabetes. Near-normal metabolic control; for 8 days induces a reduction but not a complete normalization in kidney function. From the present observations it is suggested that the rapidly reversible part of the elevation in GFR cannot be explained by concomitant changes in kidney and glomerular size (morphological origin) but is probably due to a reduction in renal plasma flow and to a decreased transglomerular pressure (functional origin).

Adult↗
PubMed1982

No response of pancreatic hormones to hypoglycemia in diabetic autonomic neuropathy.

The responses of pancreatic hormones (i.e. glucagon, pancreatic polypeptide, and somatostatin) to insulin-induced hypoglycemia were investigated in 18 insulin-dependent diabetics without residual beta-cell function and in 6 normal subjects. Nine of the diabetics had autonomic neuropathy, and 9 had no neuropathy. After hypoglycemia, no significant increase in any of the 3 pancreatic hormones was found in the diabetics with autonomic neuropathy, whereas significant increments were found in the diabetics without neuropathy and in the normal subjects. These results suggest that autonomic nervous activity is of major importance for pancreatic hormone release during hypoglycemia in man.

Adult↗
PubMed1982

Dose-dependent increase in concentrations of gastric inhibitory polypeptide and pancreatic polypeptide after small amounts of glucose intraduodenally in man.

Nine healthy volunteers were infused intraduodenally with 100 ml isotonic solutions of 1, 2.5, and 5 g glucose for 15 min at 1-h intervals. The gastric inhibitory polypeptide (GIP) concentration in plasma did not increase after 1 g of glucose, whereas after 2.5 g of glucose the GIP concentration increased from 32.1 (23.3-68.4) to 53.9 (30.0-63.0) pM and after 5 g from 36.8 (18.0-54.7) to 78.5 (46.9-163) pM. The serum concentration of pancreatic polypeptide (PP) increased only after 5 g, from 19.3 (14.8-29.1) to 28.8 (15.3-45.3) pM. This shows that the plasma concentration of GIP increases dose-dependently after small doses of duodenal glucose and that glucose really is a duodenal stimulus for an increase i serum PP concentration.

Adult↗
PubMed1982

Somatostatin-like immunoreactivity in man. Measurement in peripheral plasma.

A radioimmunoassay for the determination of somatostatin-like immunoreactivity (SLI) in plasma has been developed using antibodies raised in rabbits against synthetic somatostatin conjugated to hemocyanin and 125I-Tyr1-somatostatin. The detection limit was 2 pg/ml. A combination of EDTA and aprotinin (0.15 M and 80 Kallikrein Inhibitor Units = KIU/ml) inhibited the tracer degradation, but did not eliminate it completely. In addition somatostatin immunoreactivity in unextracted plasma showed a strong dilution effect and the estimates depended on the antiserum used (e.g. a plasma sample (1 : 5) assayed with antiserum R 141 apparently contained 150 pg/ml, whereas antiserum K 5615 yielded a value of 300 pg/ml). When plasma was extracted with acid ethanol, the values obtained with the two different antisera were practically the same, recovery of somatostatin added to plasma was approx. 80% and dilution of specimens gave proportional readings. Consequently, extraction of plasma is regarded as obligatory to ensure valid results. Mean basal level was 26.5 +/- 1.2 pg/ml (mean +/- SEM). When plasma extracts were subjected to chromatography on Sephadex G-25 at neutral pH, approx. 30% of the SLI was recovered in the MW1600 fraction; whereas the major part of the remaining immunoreactivity (37-60%) eluted earlier in one fraction and the residual immunoreactivity in the void volume.

Chromatography, Gel↗
PubMed1980

The effect of glucagon infusion on kidney function in short-term insulin-dependent juvenile diabetics.

Kidney function was studied in nine, metabolically well controlled, short-term insulin-dependent male diabetics before and during glucagon infusion of 4 to 5 and 8 to 10 ng/kg/min. Glomerular filtration rate, effective renal plasma flow (steady-state infusion technique, with urinary collections, using 125I-iothalamate and 131I-iodohippurate), and urinary albumin and beta 2-microglobulin excretion rates were measured. The mean plasma glucagon concentration increased during infusion from 254 +/- 19 pg/ml to 440 +/- 31 pg/ml (low dose) and 730 +/- 52 pg/ml (high dose). Glomerular filtration rate increased in all subjects from 133 +/- 5 before the glucagon infusion to 141 +/- 4 with the low dose, and 148 +/- 7 ml/min/1.73 m2 with the high dose (p < 0.01). The increase in glomerular filtration rate correlated with the rise in plasma glucagon concentration (r = 0.67; p < 0.01). Renal plasma flow increased from 530 +/- 21 before the glucagon infusion to 555 +/- 20 with the low dose and 572 +/- 29 ml/min/1.73 m2 with the high dose (p < 0.01). Urinary beta 2-microglobulin excretion rate rose from 5.8 +/- 1.0 before infusion to 8.7 +/- 1.7 with the low dose, and 17.9 +/- 5.7 micrograms X 10(-2)/min with the high dose (p < 0.01). Urinary albumin excretion remained unchanged during the glucagon infusion. These results suggest that glucagon may contribute to the reversible elevation of glomerular filtration rate typically found in poorly regulated insulin-dependent diabetics, but not to the moderate elevation found in well controlled diabetics.

Adolescent↗
PubMed1980

Immunoreactive glucagon and insulin C-peptide in man after resection of the pancreas and total pancreatectomy.

Pancreatic-type glucagon (PTG) has been found in the plasma of totally pancreatectomized human beings. Arginine infusion, however, caused no increase in PTG. Pancreas-resected patients had a normal response of PTG to arginine and a subnormal increase in C peptide. Gut glucagon-like immunoreactants (gut GLI) were increased in resected patients and further increased in totally pancreatectomized patients. Gut GLI showed no change during arginine stimulation.

Adult↗
PubMed1980

Gastroenteropancreatic hormonal changes during exercise.

Peripheral plasma concentrations of gastroenteropancreatic peptides were measured during a 3-h period of bicycle exercise at 40% of maximal oxygen uptake in six normal men. Marked increases (P < 0.02) were found in vasoactive intestinal polypeptide (VIP) [1.8 +/- 0.7 (rest) vs. 22.3 +/- 5.4 pmol x l-1 (mean +/- SE) (3 h)], secretin (0.5 +/- 0.5 vs. 11.1 +/- 2.7 pmol x l-1), pancreatic polypeptide (PP) (4.0 +/- 1.5 vs. 46.3 +/- 11.5 pmol x l-1), somatostatin (SRIF) (12.8 +/- 1.2 vs. 17.7 +/- 0.6 pmol x l-1), whereas no changes occurred in gastric inhibitory polypeptide (37.3 +/- 5.9 vs. 39.2 +/- 9.8 pmol x l-1). Immunoreactive insulin and C-peptide decreased from 0.08 +/- 0.004 and 0.39 +/- 0.03 pmol x l-1, respectively, to 0.04 +/- 0.003 (P < 0.005) and 0.13 +/- 0.02 (P < 0.001). The significant decrease in C-peptide and in the C-peptide-to-insulin molar ratio indicate decreased insulin secretion and clearance, respectively, during exercise. Plasma glucose decreased [5.0 +/- 0.1 (rest) vs. 4.2 +/- 0.3 mmol.l-1 (3 h)] (P < 0.01). During 3 h of rest, none of the measured parameters had changed. The marked exercise-induced changes in plasma concentrations of PP, secretin, VIP, and SRIF are provocative. We know in detail neither the stimuli for the release of these peptides nor their physiological role during exercise.

Adolescent↗