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Biomedical subjects

P Vague

Publications and source records attributed to P Vague.

At least 127 records · Page 7Linked to original sources
PubMed1987

Pancreatic polypeptide secretion in diabetic patients with idiopathic haemochromatosis.

In order to investigate the endocrine pancreatic dysfunction resulting from iron overload, plasma pancreatic polypeptide (PP) response to a protein-rich meal was studied in 10 healthy controls and 30 insulin-dependent (type I) diabetic patients: ten with idiopathic haemochromatosis (IH), ten with chronic pancreatitis and ten with idiopathic type I diabetes. While fasting plasma PP levels were slightly higher in diabetic with IH (40,8 +/- 7 pmol/l) than those in controls (27,1 +/- 3) on in type I diabetics (31,3 +/- 3) they were similar after the meal (peak level 95 +/- 18, 139 +/- 23, 100 +/- 36 respectively). In contrast the mean PP level was low in diabetics with chronic pancreatitis in the fasting state (15.9 +/- 3.6 pmol/l) and did not rise following the meal. These findings suggest that there is no PP cell injury in diabetics with IH.

Adult↗
PubMed1987

Type II diabetes in young subjects. A study of 90 unrelated cases.

Type II, non insulin dependent diabetes mellitus is commonly diagnosed after the age of 45 years. For this reason it was previously called maturity onset diabetes. Type II diabetes occurring in young subjects has generally been described in selected pedigrees. The purpose of this work was to review data from all the unrelated type II diabetics (with fasting hyperglycemia) diagnosed before the age of 45 and observed in our department over the last four years. A total of 90 such patients including 44 men and 46 women were included in this study. Of 43 cases diagnosed before the age of 30, there were 30 women compared to only 16 women out of 47 cases diagnosed between 30 and 45 years (p less than 0.001). At the time of diagnosis 42 patients had a relative body weight lower than 120%. In 66,7% of the cases, one parent was a known diabetic. The rate of diabetes in the sibships was 50%. Differences in family history of diabetes were not observed in relation to age or weight at diagnosis. Comparison with a series of 150 conventional type II diabetics in whom diagnosis was made between 45 and 60 years of age showed a significantly greater frequency of obesity (86%) and fewer diabetic parent (36%). The mean apparent duration of diabetes was 14 years (range 5-42). Microangiopathy was not infrequent in these diabetic patients. Twenty-three patients had retinopathy, proliferative in 8 cases, and 3 were blind. Nine had renal insufficiency, severe in 3 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Rapid modifications of biophysical and biochemical parameters of red blood cell membrane from insulin dependent diabetics after insulin administration.

We have previously shown that red blood cell (RBC) filtrability in uncontrolled insulin dependent diabetics is abnormal compared to healthy subjects, but is corrected by insulin added in vivo or in vitro. We have now found biophysical abnormalities of the RBC membrane in such patients: Fluorescence polarization value (p) evaluated using DPH as probe is significantly lower in patients; insulin added in vitro increases and normalises the p value of diabetic RBC membrane, and has no effect on normal RBC membrane. As there is a relationship between the lipid bilayer and membrane cytoskeleton proteins, this abnormality of RBC membrane fluidity, correctable by insulin, may be an important determinant of the rheological behaviour of the RBC. In parallel, biochemical abnormalities of the RBC membrane are shown in the same patients: Higher cholesterol/phospholipid ratio, lower content in unsaturated fatty acids and higher content in saturated fatty acids. Decreased activity of ouabaine sensitive Na+K+ ATPase and increased activity of Mg++ ATPase. All of these RBC biochemical abnormalities are corrected after 24 h of normoglycaemia obtained by insulin treatment given in vivo with a biostator. Our results show the importance to check the degree of control of glycaemia when studying rheological parameters in diabetes mellitus.

Ca(2+) Mg(2+)-ATPase↗
PubMed1986

Correction by insulin added in vitro of abnormal membrane fluidity of the erythrocytes from type 1 (insulin-dependent) diabetic patients.

Filtrability of erythrocytes obtained from uncontrolled Type 1 (insulin-dependent) diabetic patients is abnormal, but is corrected by insulin added in vivo or in vitro. As erythrocyte filtrability depends on several determinants, we chose to study a membrane property of erythrocytes from diabetic subjects. Membrane fluidity was studied by fluorescence polarization using a lipophilic probe, the diphenyl-hexatriene and the Coulter Epics V together with a laser Spectra-physics 2000. Fluorescence polarization values obtained for 31 normal subjects (0.253 +/- 0.043 SD) and 31 uncontrolled Type 1 diabetic patients (0.231 +/- 0.043 SD) were significantly different (p less than 0.01). Insulin (2.5.10(-9) mol/l) added in vitro increased the fluorescence polarization values of red cell membranes from diabetic patients (without insulin, fluorescence polarization values = 0.210 +/- 0.032 SD; with insulin, fluorescence polarization values = 0.253 +/- 0.024 SD, p less than 0.001, n = 15), but had no effect on normal membranes (without insulin fluorescence polarization values = 0.255 +/- 0.037 SD, with insulin, fluorescence polarization values = 0.251 +/- 0.026 SD; n = 12). Given a relationship between the lipid bilayer and membrane cytoskeleton proteins, this insulin-correctable abnormality of erythrocyte membrane fluidity may be an important determinant of the rheological behaviour of erythrocytes from diabetic patients.

Adult↗
PubMed1986

Correlation between blood fibrinolytic activity, plasminogen activator inhibitor level, plasma insulin level, and relative body weight in normal and obese subjects.

This study was undertaken to obtain further information on the mechanism by which blood fibrinolytic activity, a balance between plasminogen activators and inhibitors, is lowered in obese subjects. Fasting blood samples were collected from 35 subjects, aged 15 to 45 years, with normal glucose tolerance and a Body Mass Index (BMI) varying widely between 16 and 45 (normal, 19 to 25). Euglobulin Fibrinolytic Activity (EFA) did not correlate with the level of tissue type plasminogen activator (t-PA) related antigen but exhibited a negative correlation with the level of PA inhibitor (r = -.609, P less than 0.01). EFA was negatively and PA inhibitor positively correlated with both BMI (r = -.381, P less than 0.02 and .664, P less than 0.01, respectively) and plasma insulin level (r = .410, P less than 0.02 and .521, P less than 0.01, respectively). Stepwise analysis showed that these correlations were independent. As expected, plasma insulin was correlated with BMI (r = .512, P less than 0.01) and triglyceride level (r = .38, P less than 0.02), total cholesterol with age (r = .379, P less than 0.02). Ten obese subjects were submitted to a 24-hour fast. While body weight did not change appreciably, plasma insulin decreased from 22.3 +/- 2.2 to 16.3 +/- 1.1 microU/ml, EFA increased from 3.6 +/- .8 to 4.9 +/- .67 mm, and PA inhibitor decreased from 4.52 +/- .76 to 3.44 +/- .63 IU/mL. All these differences were significant. T-PA-related antigen did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Mechanism and significance of insulin resistance in myotonic dystrophy.

In order to elucidate the mechanism of the glucose intolerance frequently associated with myotonic dystrophy (MD), glucose metabolism of 10 patients and 10 controls was investigated using the following tests: successive intravenous stimulation of insulin secretion by glucose and tolbutamide, detection of serum islet cell antibodies, measure of the specific insulin binding on erythrocytes and evaluation in vivo of insulin sensitivity by the euglycaemic glucose clamp method. Glucose tolerance was decreased in MD patients (K value: 1.51 +/- 0.15 vs 2.4 +/- 0.2 X 10(-2)) in spite of a basal (26 +/- 4 vs 11 +/- 2 microU/ml) and post-stimulative hyperinsulinism (area of the plasma insulin curve after glucose IG: 642 +/- 120 vs 315 +/- 28 microU/ml/min and area after tolbutamide IT: 740 +/- 166 vs 335 +/- 35 microU/ml/min). No islet cell antibody was detected in the serum of MD patients. These results suggest that decrease of glucose tolerance is secondary to peripheral insulin resistance. Specific binding of insulin on erythrocytes was slightly but not significantly reduced in MD patients (specific binding: 8.21 +/- 0.9 vs 9.64 +/- 0.9%, receptor number: 23 +/- 2 receptors/cell, concentration of unlabelled insulin displacing 50% of the bound radioactivity: 7.2 +/- 0.56 vs 6.6 +/- 0.6 ng/ml). There was a loss of normal down regulation of insulin receptors in MD. The results of the euglycaemic glucose clamp confirmed the insulin resistance especially for the highest insulin infusion rates. These data show that the insulin resistance of MD is due to both receptor- and post receptor-defect but that the main abnormality is an unresponsiveness located after the insulin signal on the receptor.

Adult↗
PubMed1985

Increased PA-inhibitor levels in the postoperative period--no cause-effect relation with increased cortisol.

It has been reported that the level of PA-inhibitor increases in postoperative patients and on the other hand that glucocorticoids increase the PA-inhibitor level in cell culture. Because surgery is associated with increased plasma cortisol level, a relation between the postoperative increase in plasma cortisol and PA-inhibitor levels was looked for. Blood samples were collected from 8 patients undergoing extensive abdominal surgery, before operation and postoperatively at 2 hr, 4 hr, 24 hr and daily for 7 days. Plasma cortisol and PA-inhibitor were increased 2 hr after surgery, when there was a significant correlation (p less than 0.05). The maximum increase was at 24 hr and the values fell to normal on day 6. An increase in t-PA related antigen (t-PA R:Ag) and a decrease in euglobulin fibrinolytic activity (EFA) also occurred. In 7 controls 0.25 mg ACTH was given intravenously and blood was collected after 1/2, 1, 2, 4, 6 hr. Although the increase in plasma cortisol level following ACTH was comparable to that observed after surgery the increase was not associated with significant change in PA-inhibitor level, t-PA R:Ag or EFA. A cause-effect relationship between the increased plasma cortisol and PA-inhibitor level could not be shown. The mechanism of the postoperative increase in PA-inhibitor thus remains unknown.

Abdomen↗
PubMed1985

Possible participation of adenosine 5'-diphosphate, arachidonic acid and paf-acether in the platelet pro-aggregating effect of uncontrolled insulin-dependent diabetic erythrocytes in vitro.

The red blood cells (RBC) from uncontrolled insulin-dependent diabetics (U.IDD) induce aggregation of platelets from control subjects. This effect was not observed when using platelets made unsensitive to adenosine 5'-diphosphate (ADP), arachidonic acid (AA) or paf-acether. Since RBC from U.IDD are less deformable than those from control subjects, we treated normal RBC in vitro with glutaraldehyde. These rigid RBC were used to study aggregation of normal platelets and of those unsensitive to ADP, AA or paf-acether. Results obtained with glutaraldehyde-treated RBC were comparable to those obtained with RBC from U.IDD, i.e. aggregation was obtained with untreated platelets but not with platelets unsensitive to ADP, AA or paf-acether. It is hypothesized that aggregation of control platelets induced by RBC from U.IDD is purely mechanical at its origin but is ultimately mediated by ADP, AA or paf-acether.

Adenosine Diphosphate↗
PubMed1985

Impaired pancreatic polypeptide response to insulin hypoglycemia in obese subjects.

We have studied the effect of insulin hypoglycemia on the secretion of pancreatic polypeptide (PP) in 14 obese subjects with normal glucose tolerance and in 6 normal controls. Infusion of insulin 0.1 U/kg/h in controls and 0.12 U/kg/h in the obese, for one hour, produced a progressive hypoglycemia, similar in both groups (nadir 2 mmol/l at 50 min). The secretion of PP was less in obese subjects than in controls (peak 116 mmol/l vs 184 pmol/l, P less than 0.01) (integrated secretion sigma delta PP 288 vs 472 pmol/l, P less than 0.01) and was also delayed in the obese subjects beginning at 50 min instead of 40 min. The secretion of glucagon and of C-peptide were not different in the two groups, but the integrated response of ACTH was higher in the obese (sigma delta ACTH 52 pmol/l vs 25 pmol/l, P less than 0.01). The secretory response of growth hormone (STH) was smaller in the obese group (peak 8.6 +/- 1.28 vs 21.4 +/- 6.4 ng/ml, P less than 0.01). The reduced secretion of PP in obese subjects could be due to impaired sensitivity to hypoglycemia of the central control mechanism for PP release. The similarity of the reductions in the secretion of both PP and STH support this hypothesis, although a reduction in the secretory capacity of pancreatic PP cells cannot be excluded.

Adrenocorticotropic Hormone↗
PubMed1985

HLA-A, B, DR antigens and insulin-dependent diabetes in Algerians.

HLA-A, B and DR antigens have been investigated in insulin-dependent diabetics and compared to controls in a population of Algerians. A decrease of A1 and DR2 and an increase of Aw 19.2; B8, B18 and especially DR3 were found in diabetics in comparison to controls. The strongest association was found for DR3, which is a good genetic marker of IDD (RR = 8.50) in this population. The frequency of some HLA antigen associations in IDD suggests that the diabetic gene(s) is linked to 2 main haplotypes: Aw 19.2; B18; DR3 and Aw 19.2; B8; DR3. Antigen DR4 was equally represented in IDD (21%) and controls (28.4%), but heterozygote DR3-DR4 was more frequent in diabetics. The relation between IDD and HLA antigens found in the Algerian population is very similar to that described in diabetic Caucasian populations of southern Europe, except for the lack of association with DR4.

Adult↗
PubMed1985

[Initial remission period in insulin-dependent diabetes in the young subject].

Occurrence of a remission after initiation of insulin treatment in insulin dependent diabetes (type I) of recent onset is a well known phenomenon. It may be more or less complete up to insulin withdrawal. In newly diagnosed IDD requiring insulin for ketoacidosis or primary failure of oral agents and with a duration of symptoms of less than 6 months, initiation of optimized insulin therapy was followed by suppression of insulin (with or without the use of oral agents) in two thirds of cases for a mean period of 12 months while blood glucose and glycosylated haemoglobin remained normal. As therapeutic reversal of the etiopathological mechanism of IDD is foreseen it is relevant to define the characteristics of cases with remission induced by intensified insulin treatment, and the mechanisms by which they may be explained. Current knowledge on these questions will be analysed in this review. Furthermore it appears that withdrawing insulin for a mean period of 12 months does not hamper the subsequent control of diabetes.

Adolescent↗
PubMed1984

[Specific immunologic resistance to bovine insulin in an insulin-dependent diabetic].

A 60-year old male diabetic patient treated with insulin for 6 years developed ketosis whenever an attempt was made to replace porcine insulin by mixed bovine and porcine insulin. That this resistance was specific to bovine insulin and of immune origin was demonstrated by in vivo and in vitro studies. The in vivo study used a Biostator artificial pancreas: rapid decrease of plasma glucose concentrations was observed under insulin infusion at a constant rate of 200 mU/min with either porcine or semi-synthetic human insulin despite maximum glucose infusion rate (400 mg/min), but not with bovine insulin and a low glucose infusion rate (150 mg/min). In the in vitro study, high levels of anti-insulin antibodies (11.4 m U/ml, Christiansen method) were found in the plasma, and the curves of competitive binding of radiolabelled insulin to the patient's IgG in the presence of unlabelled porcine or bovine insulin showed a 50% decrease of total binding with 0.12 ng/ml of bovine insulin and 25 ng/ml of porcine insulin, suggesting that the affinity of these antibodies for the former was 200 times higher than for the latter.

Animals↗
PubMed1984

Effect of 24 hours of normoglycaemia on tissue-type plasminogen activator plasma levels in insulin-dependent diabetes.

We have previously demonstrated that a short period of normoglycaemia obtained through an artificial pancreas in uncontrolled insulin-dependent diabetics improves parameters of the functional microangiopathy such as erythrocyte deformability and platelet aggregation. Because recently an immunoradiometric assay for tissue plasminogen activator (t-PA) was developed we measured t-PA levels in 18 uncontrolled insulin-dependent diabetics before and after 24 hr of normoglycaemia induced by insulin to look for a modification of endothelial cells function. After 24 hr of strict control, plasma free insulin levels rose significantly, total t-PA R-Ag, its active fibrin binding fraction and euglobulin fibrinolytic activity were significantly decreased. These results suggest a responsibility for insulin in the decrease in t-PA blood level and could explain at least partially the relation between hyperinsulinism, thrombosis and atherogenesis.

Adolescent↗