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P Vague

Publications and source records attributed to P Vague.

At least 145 records · Page 8Linked to original sources
PubMed1984

Anti-tubulin antibodies in recent onset type 1 (insulin-dependent) diabetes mellitus: comparison with islet cell antibodies.

Antibodies to tubulin, the fundamental protein of microtubules, were studied by radioimmunoassay in patients with Type 1 (insulin-dependent) diabetes of varying duration and in healthy control subjects. Elevated levels of anti-tubulin antibodies were found in 46% of 28 patients with Type 1 diabetes of recent onset (less than or equal to 6 months) and in only 6.2% of 64 patients with long-standing Type 1 diabetes (duration 6-43 years). None of 34 DR3-positive normal subjects and none of 20 Type 2 (non-insulin-dependent) diabetic patients were positive for anti-tubulin antibodies. Anti-tubulin antibody levels were elevated in two out of 26 first-degree relatives of Type 1 diabetic patients. The specificity of the detection of anti-tubulin antibodies was demonstrated by dilution of the sera, competitive binding experiments between labelled and unlabelled tubulin, immunoblotting. Antibodies to tubulin were elevated in 60% of patients with islet cell surface antibodies and there was a significant association between anti-tubulin antibodies and islet-cell surface antibodies. These antibodies, however, recognize different specificities, since adsorption of islet cell surface antibody by rat islets did not alter the anti-tubulin antibody activity. Elevated anti-actin antibody responses were found in two out of 17 and one out of 26 patients with recent onset and long-standing Type 1 diabetes, respectively. In conclusion, anti-tubulin antibodies are detected in a high proportion of patients with diabetes of recent onset, are associated with islet cell surface antibodies and like islet cell surface antibodies decrease or disappear during the course of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1983

[Comparison of various types of islet cell antibodies in diabetes as a function of its cause and duration].

Three types of pancreatic islet cell antibodies (ICA) have been described in insulin-dependent diabetic patients: IgG-ICA directed against cytoplasmic antigens, complement-fixing antibodies (CF ICA) and islet cell surface antibodies (ICSA) directed against membrane antigens. They can be detected by indirect immunofluorescence methods using human pancreas sections for IgG-ICA and isolate rat live islet cells for ICSA. Distribution of these 3 types of antibodies and correlations within individual patients were investigated in non-diabetic controls, in patients with idiopathic diabetes of various duration and in patients whose diabetes was associated with autoimmune diseases, chronic pancreatitis or haemochromatosis. The respective incidences of IgG-ICA and ICSA were: 5.4% and 15.8% in controls, 67.3% and 64.3% in patients with recent onset diabetes, 22.6% and 21.5% in old-standing diabetes, 63% and 50% in auto-immune diabetes, 12.5% and 7.2% in diabetes from chronic pancreatitis, and 5.6% and 7.6% in diabetes from haemochromatosis. In contrast with these correlations within groups, individual concordances were only 67%. CF ICA were relatively rare and almost exclusively present in IgG-ICA positive patients (30% of all cases); they seem to constitute a sub-group of IgG-ICA. It is concluded that IgG-ICA and ICSA are equally frequent in each type or duration of insulin-dependent diabetes and that they are not associated with secondary diabetes. The lack of concordance in individual patients indicates that the anti-pancreatic immune response is not homogeneous.

Adult↗
PubMed1983

[Evaluation of the acceptability of 2 methods for self monitoring of blood sugar by a group of insulin-dependent diabetic patients].

In order to evaluate the advantages and disadvantages of two methods of blood glucose self-monitoring (either direct semi-quantitative reading on Haemoglukotest 20-800 or quantitative reading of Dextrostix strips using a reflectance-meter, Glucometer) 20 insulin-dependent diabetics selected according to the quality of the management of their own diabetes were asked to try both methods for 3 months and then fill a questionnaire assessing their acceptance. Analysis of the responses shows that home blood glucose monitoring is well accepted even after one year by patients aware of the necessity of a good glycemic control. It is specially useful for the adaptation of insulin doses and less so for identification of hypoglycemic attacks. Haemoglukotest 20-800 is appreciated for its easy utilization specially during professional life and outside leisure. However, the reflectance-meter Glucometer is preferred by most patients because they feel it is more reliable and safe.

Adolescent↗
PubMed1983

Clinical features of diabetogenic and atherogenic obesity.

Fat mass per se has little effect on the progression of obesity towards diabetes. Predominance of fat in the upper part of the body resulting in android obesity is at least the clinical reflection of factors which lead obesity to progress towards diabetes and atherosclerosis. Therefore, this type of obesity may be termed diabetogenic and atherogenic obesity. Insulin and cortisol secretion in obesity are not correlated with body fat but with the predominance of fat in the upper part of the body. Diabetogenic obesity may evolve through 5 stages from initial obesity without diabetes to insulin dependent diabetes in previously obese subjects. Aside from the characteristics of body fat distribution, the mechanisms which induce or interrupt this progression remain unknown.

Adolescent↗
PubMed1983

Red cell deformability, platelet aggregation, and insulin action.

Abnormalities of rheologic and hemostatic properties of blood are present in uncontrolled diabetics and play a role in the development of structural micro- and macroangiopathies. Red blood cell deformability is decreased in diabetics and shows negative correlation with fast hemoglobin and actual blood glucose levels. In uncontrolled insulin-dependent diabetics, normalization of plasma glucose by an insulin infusion improves red cell deformability in 2 h. Insulin infusion (0.2 U/kg/h) [the initial hyperglycemia being maintained (hyperglycemic clamp)] also improves red cell deformability. Deformability of normal erythrocytes is reduced by incubation in plasma from uncontrolled diabetics but is normal in plasma from diabetics controlled by a 24-h insulin infusion or in diabetic plasma with insulin added in vitro. Therefore, insulin appears to have a direct effect on erythrocyte deformability. Platelet aggregation measured in whole blood is raised in uncontrolled diabetics. Aggregation of normal platelets rises in the presence of "diabetic" red cells but not in the presence of red cells from the same patients controlled by 24-h treatment with insulin. The effect of insulin on platelet aggregation, therefore, seems to be at least partly mediated by erythrocytes.

Adenosine Diphosphate↗
PubMed1983

Assessment of viral and immune factors in EMC virus-induced diabetes: effects of cyclosporin A and interferon.

EMC virus-induced diabetes in mice may be a model of human type I diabetes. It is postulated that auto-immune reaction plays a role in beta cell destruction after viral aggression. The use of anti-viral (interferon) or immunosuppressive drugs (Cyclosporin A) could contribute to an understanding of the pathogenesis of diabetes in this model. Early or late administration of cyclosporin A increased mortality and frequency of diabetes in female mice and did not influence these parameters in males despite a reduction of pancreatic inflammatory lesions. Interferon administered at the time of virus inoculation diminished mortality in both sexes and frequency of diabetes in males. These results are against an autoimmune pathogenesis for diabetes in this model and suggest that the virus plays the major role in beta cell damage.

Animals↗
PubMed1983

Overnight basal insulin requirements in insulin dependent diabetics.

Programming open loop insulin delivery systems makes necessary the knowledge of patients insulin needs. It is frequently postulated that insulin needs increase at the end of the night in relation to the rise in cortisol secretion. According to this hypothesis is it justified to speed up the insulin infusion rate in the early morning? This question was addressed by studying insulin infusion rate by an artificial pancreas during the night in 12 C. peptide negative insulin dependent diabetics. They were connected to the artificial pancreas from 8 a.m. to 10 a.m. the next morning while on their habitual diabetic diet and slept as usual from 11 p.m. to 7 a.m. approximately. From 11 p.m. to 7 a.m. mean insulin infusion rate was 21.5 +/- 3.3 mU/Kg/h representing 15.6 +/- 1.6% of the dose delivered in 24 hours. Blood glucose was stable around 85 mg/dl. No significant differences were observed in the hourly insulin infusion rate during the night period, in spite of a slight tendency to a rise (from 21.1 +/- 2.8 to 22.1 +/- 2.6 mU/kg/h) tendency to a rise (from 21.1 +/- 2.8 to 22.1 +/- 2.6 mU/kg/h) after 4 a.m. On the basis of these results obtained in patients sleeping as usual it does not appear useful to envisage a systematic acceleration of insulin infusion rate by continuous delivery systems in the early morning.

Adult↗
PubMed1983

[Decrease in the serum level of the C3 complement component in noninsulin dependent diabetes of recent onset].

Complement components C3, C4 and C3A were measured by immuno-diffusion in plasma of 36 recent onset insulin-dependent diabetics (IDD) and compared to plasma complement levels of 19 long-standing IDD and 18 non diabetic controls. A significant decrease of C3 and a mild increase of C3A was found in recent-onset diabetes group. However these variations could not be correlated with IgG-islet cell antibodies, C3--fixing islet cell antibodies or A--B HLA antigens. No significant difference was found between long-standing IDD and controls for the 3 complement components. In conclusion, the decrease of C3, found in 30% of recent onset IDD, might be due to increase complement consumption either by the insulitis process or by circulating immune complexes.

Adolescent↗
PubMed1982

[The artificial pancreas in surgery. An attempt to simplify intra- and post-operative insulin therapy].

The insulin requirements of 10 insulin-dependent diabetic patients were evaluated during and after surgery (including 4 caesarian sections) by connecting the patients with an artificial pancreas. Considerable variations were observed in the intra-operative period. In contrast, the amounts of insulin released during the immediate post-operative period were more regular and reproducible (mean: 2.36 U/h for a glucose intake of 200-250 g/24 h). A satisfactory control of glycaemia was obtained with this dosage in 7 insulin-dependent post-operative patients without using an artificial pancreas. It would therefore seem that in most cases continuous insulin infusion combined with direct measurement of capillary glycaemia could replace an artificial pancreas and make the intra- and post-operative care of diabetic patients simpler and more effective.

Adult↗
PubMed1982

Abnormalities of erythrocyte deformability and platelet aggregation in insulin-dependent diabetics corrected by insulin in vivo and in vitro.

Erythrocyte deformability is lower than normal in uncontrolled insulin-dependent diabetics and returns towards normal after 24 h treatment with a feedback-controlled insulin infusion. Deformability of normal erythrocytes is reduced by incubation in plasma from uncontrolled insulin-dependent diabetics but is normal in plasma from insulin-dependent diabetics controlled by 24 h insulin infusion, or in plasma from uncontrolled insulin-dependent diabetics with insulin added in vitro. Therefore, insulin has a direct action on erythrocyte deformability. Platelet aggregation measured in whole blood is raised in uncontrolled insulin-dependent diabetics and returns to normal after 24 h treatment with a feedback-controlled insulin infusion. Aggregation of normal platelets rises in the presence of erythrocytes from uncontrolled insulin-dependent diabetics, but not erythrocytes from the same patients after 24 h treatment with insulin. The effect of insulin on platelet aggregation therefore seems to be at least partly mediated by erythrocytes. The enhanced platelet aggregation seen in uncontrolled insulin-dependent diabetics can be explained either by a direct effect of erythrocyte rigidity or by an increased release of nucleotides (ADP) by the erythrocytes.

Diabetes Mellitus↗
PubMed1982

Kinetics of fast haemoglobin in diabetic rats.

This study was designed to examine the appearance and disappearance kinetics of glycosylated haemoglobin during abrupt changes of blood glucose in the rat. The concentration of the fast haemoglobin component, which has similar chromatographic and electrophoretic profiles to human haemoglobin A1, was measured after the induction of diabetes by streptozotocin and its cure by syngeneic intraportal islet transplantation. Fast haemoglobin was increased in 12 diabetic rats compared with 22 controls (15.8 +/- 0.8 versus 8.2 +/- 0.3%, mean +/- SEM). In a group with mild diabetes (n = 8, blood glucose less than 22 mmol/l), fast haemoglobin rose to 13.7 +/- 1.0% by week 8. In a group with severe diabetes (n = 4, blood glucose greater than 22 mmol/l), fast haemoglobin rose more quickly (in 3 weeks) to a higher level (18.2 +/- 3.3%) and changed little thereafter. This suggests a saturable system in which the rate of increase and final value depend upon the degree of hyperglycaemia. After islet transplantation, fast haemoglobin returned to normal in 4 weeks (n = 5, 17.6 +/- 1.4 to 9.4 +/- 0.9%). This delay is shorter than expected from the red cell lifespan (around 60 days), suggesting that haemoglobin glycosylation may be partly reversible. These results suggest that in unstable diabetes the interpretation of haemoglobin A1 levels is not as simple as was supposed previously.

Animals↗
PubMed1982

The defective glucose sensitivity of the B cell in non insulin dependent diabetes. Improvement after twenty hours of normoglycaemia.

In non insulin dependent diabetics (N.I.D.D.) of normal body weight, the acute insulin response to glucose is defective while that to pharmacologic agents such as tolbutamide is less impaired. This specific B-cell insensitivity to glucose results from unknown and perhaps multiple mechanisms. Hyperglycemia may be itself aggravate this phenomenon. To test this hypothesis acute insulin release (delta I: sum of increment at 2, 5, 10 min) after intravenous and tolbutamide injection was studied in 5 N.I.D.D. with fasting blood glucose averaging 12.1 mM/I (range 10.7-13.7) before and after 20 hours of glycemic normalization by an artificial pancreas. Intravenous injection of .3 g/k glucose did not elicit an acute insulin or C-peptide response, but following Tolbutamide (20 mg/kg) delta I was 44 +/- 21 microU/ml and delta C-peptide 0.84 +/- 0.37 nM/I. After 20 hr of normoglycemia a response to glucose was apparent (delta I 60 +/- 24 and delta CP 0.86 +/- 26) that to Tolbutamide was unchanged (delta I 58 +/- 26 and delta CP 0.97 +/- 0.27). These results suggest that 20 hr of normoglycemia improve significantly the "glucoreceptor" function of the B-cell in N.I.D.D.

Adult↗
PubMed1982

[Effects of strict control of blood sugar by an artificial pancreas on nerve conduction velocity in diabetics].

This study concerned 13 patients with diabetes mellitus who, although under insulin therapy treatment, had poor control of their diabetes. Motor conduction velocity (MCV) in the peroneal, ulnar and median nerves, sensory conduction velocity (SVC) of the median nerve and sensory potential amplitude (SPA) of the median nerve were determined immediately before and after 24 h of strict control of blood glucose by an artificial pancreas. A significant increase in the MCV of the ulnar nerve (P less than 0.01) and in the SCV of the median nerve (P less than 0.05) was found. This acute improvement led us to presume that repair of anatomic lesions would be extremely unlikely. Only a metabolic disturbance due to hyperglycemia can be rapidly corrected. This metabolite alteration may be held partly responsible for the slowing of nerve conduction in diabetes. No significant difference was noted in the MCV of the peroneal nerve and of the median nerve and the SPA of the median nerve. This suggests that advanced degenerative lesions are present in these nerves particularly in the lower limbs. Such lesions cannot be rapidly reversed by metabolic control.

Adolescent↗
PubMed1982

[Erythrocyte and platelet parameters and degree of control of diabetes].

There are abnormalities of haemostasis and rheological properties in uncontrolled diabetics which could well be involved in the pathogenesis of diabetic microangiopathy and macroangiopathy. Erythrocyte deformability was reduced with a negative correlation with the degree of control (blood sugar and glycosylated hemoglobin). In uncontrolled insulin dependent diabetics (IDD), returning blood sugar to normal with a continuous infusion of insulin using an artificial pancreas, improved deformability in several hours; even if the raised blood sugar was maintained artificially, a perfusion of insulin and still had the same effect; the poor erythrocyte deformability in IDD seems therefore to be related more to the level of insulin than to hyperglycaemia. This finding was confirmed in vitro: normal erythrocytes incubated in plasma from uncontrolled IDD had a low deformability, the addition of insulin in physiological concentration prevented this; after incubation for 3 h at 37 degrees C in the absence of insulin, erythrocyte deformability was low whereas in the presence of insulin, normal deformability was maintained. Platelets from IDD showed increased aggregation when measured in whole blood. This phenomenon seems to be mediated by erythrocytes because normal platelets became hyperagregable in the presence of "diabetic" erythrocytes.

Blood Glucose↗
PubMed1982

[Auto-immunity and insulin-dependent diabetes].

Many observations suggest that auto-immune process are activated during the beta-cell destruction in insulin-dependent diabetes (IDD): they include association with organ specific auto-immune disease, frequency of circulating anti-organ antibodies, circulating anti-islet cell antibodies, insulitis-like lesions in the pancreas and in vitro lymphocytic reaction against pancreatic antigens. However, it is still uncertain if these reactions are actually involved in the beta cell destruction. Cytotoxicity experiments on beta cells in culture and animal models support this hypothesis. Nosologic classification which categorizes an autoimmune type of IDD, a viral type of IDD and a large proportion termed idiopathic IDD may be a useful device to further our understanding of the pathogenic pathways but may be open to criticism of undue simplification as in this presumably multifactorial disease, the differences between affected individuals may be quantitative and not qualitative.

Animals↗