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Biomedical subjects

R Assan

Publications and source records attributed to R Assan.

At least 109 records · Page 6Linked to original sources
PubMed1982

[New insulins].

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Animals↗
PubMed1981

[Inhibition of insulin secretion in vitro by serum of diabetic subjects in the presence of complement].

In order to explore complement-dependent humoral immunity in insulin-dependent diabetic patients, their serum was incubated with Mouse isolated pancreatic islets in the presence of complement, after which the response of these islets to glucose was estimated by measuring insulin secretion. Out of 13 sera from insulin-dependent diabetic patients, 5 caused a significant inhibition of the insulin response. Morphological observation of islets suggested that this inhibition was due to a cytotoxic effect of the sera. In the absence of complement, the same sera were not able to suppress insulin release. No beta-cell inhibition or morphological damage was detectable on islets incubated with sera from 13 healthy subjects and 4 non-insulin dependent diabetic patients, in the presence or in the absence of complement. Complement-dependent humoral immunity may play a role in the beta-cell injury of insulin-dependent diabetes.

Animals↗
PubMed1981

Lymphocytes from diabetics suppress insulin release in vitro.

The insulin response of isolated islet cells to glucose and theophylline in vitro was studied after incubation with lymphocytes. The test was employed to explore cell-mediated immunity in diabetics. A significant inhibition of insulin response to glucose and theophylline as compared to insulin release in a "basal" medium was found after incubation with blood lymphocytes from 21 out of 23 insulin-dependent diabetics (mean secretion index 18 +/- 18 versus 118 + 8 (SEM) % in control subjects). Most of the patients studied had associated autoimmune diseases: all of these displayed inhibition of insulin release. In six cases, the diabetes had a recent onset with no associated autoimmune disease: four of them displayed the same inhibition. No inhibition was found in the 26 control subjects and in seven non-insulin-dependent diabetics (mean secretion index 134 +/- 17 versus 145 +/- 23 (SEM) % in four control subjects). Lymphocytes inhibiting islet cell response were not cytotoxic against mouse fibroblasts. Twenty-two insulin-dependent diabetics showed islet cell antibodies to human and/or mouse pancreatic islets. However, an inhibition of insulin release was found with no detectable islet cell antibodies in one case, and the converse in two cases. Lymphocyte cytotoxicity to islet cells could play a role in the natural history of insulin-dependent diabetes.

Adolescent↗
PubMed1981

Minor hemoglobin components in diabetic and uremic patients.

Hemoglobins A1c and A1a+b were measured by an automated chromatographic method in 11 control subjects, 100 diabetics and 30 subjects with renal failure not induced by diabetes. Hb A1c was higher in diabetics than in controls (8.26 +/- 0.31 versus 5.24 +/- 0.28, p less than 0.01) and strongly correlated with blood glucose values for the preceding 4 months. In poorly controlled diabetics, submitted to an intensive therapeutic program, Hb A1c decreased rapidly. Hb A1c was slightly but significantly elevated in the uremic, non-diabetic patients who were not submitted to periodic hemodialysis: 6.42 +/- 0.32, p less than 0.05. It returned, in hemodialyzed patients, to a level not significantly different from the control value. Hb A1a+b was elevated in diabetic subjects (2.43 +/- 0.04 vs. 1.55 +/- 0.01 in controls, p less than 0.001). It was also higher in the uremic patients (2.71 +/- 0.14, p less than 0.001). No decrease occurred in the hemodialyzed patients (3.27 +/- 0.31). Glycosylated hemoglobin values, as routinely estimated and expressed under the name of "Hb A1", should be interpreted with caution in patients with renal failure. Methods discriminating Hb A1a+b have to be used.

Diabetes Mellitus↗
PubMed1981

Plasma glucagon and insulin concentrations and hepatic phosphoenolpyruvate carboxykinase and pyruvate kinase activities during and upon adaptation of rats to a high protein diet.

Plasma hormones, glucose and free fatty acids, liver glycogen and two key enzymes of glycolysis and gluconeogenesis were examined in adult rats during a 40-day period of high protein feeding. Plasma insulin fell within 1 day but returned to normal after 4 days. Glucagon changed more slowly, reaching a maximum on day 4 and declined to near the control value within 24 days. Consequently, the insulin to glucagon ratio was lower on days 1, 4 and 8 and was nearly normal on day 24. With respect to hepatic enzymes, phosphoenolpyruvate carboxykinase activity rose sharply on the 1st day and remained elevated for 40-day period; the L-isozyme of pyruvate kinase, although unchanged on the 1st day, decreased thereafter and from day 8 on represented 15--20% of control. Circadian variations in these parameters were also measured in rats adapted to the high protein diet. In such animals, the diurnal change in plasma hormones was less marked but tended to be inverted with respect to controls; the insulin/glucagon ratio was highest during daylight on high protein and in late night on the control diet. Over 24 hours, pyruvate kinase activity was related directly and phosphoenolpyruvate carboxykinase inversely to the hormone ratio. We concluded that in rats adapted to high protein, as in controls, the diurnal balance between glycolysis and gluconeogenesis is probably regulated by the same factor, namely the insulin/glucagon ratio.

Animals↗
PubMed1981

Growth and metabolic and hormonal profiles during transpyloric and nasogastric feeding in preterm infants.

The effect of transpyloric and nasogastric feeding on the blood concentration of glucose, lactate, pyruvate, glycerol, hydroxybutyrate, acetoacetate, alanine, insulin, pancreatic and total glucagon was determined in 20 preterm infants. The babies were studied on the last day of transpyloric feeding and the first and fifth days of ensuing nasogastric feeding. In 9 infants hourly measurements of hormones and metabolites were made at 1000, 1100, 1200, 1300 and 1400 hours. The blood concentrations of glucose, alanine, pancreatic and total glucagon were stable, the concentration of the other metabolites and insulin, less so. No significant difference in mean metabolite or hormone concentration was noted by time of day or type of feeding. Measurements made on the fifth day of nasogastric feeding showed no significant differences from those at the time of changeover. The infants were clinically well and growing normally at the time of study, but had low plasma insulin and high plasma glucagon concentrations. We conclude (i) the site of presentation of milk in the gastrointestinal tract has no effect on the circulating concentration of selected metabolites and hormones in the preterm infants, (ii) the preterm infant grows at a normal rate with a plasma insulin/glucagon ratio that in the adult would be expected to favour catabolism.

Alanine↗
PubMed1981

Complement-fixing Islet cell antibodies from some diabetic patients alter insulin release in vitro.

To explore humoral immunity in insulin-dependent diabetic (IDDM) patients, we studied insulin release from isolated mouse islets stimulated by glucose + theophylline after incubation with the sera of these patients and complement. Eleven of 21 IDDM sera suppressed the stimulated insulin release while the arginine-stimulated glucagon release remained unchanged. Morphologic evidence and the trypan-blue exclusion test suggested that the suppression of insulin release was due to a cytotoxic effect of the sera. No beta-cell inhibition of morphologic damage was detectable in the presence of sera from 30 healthy subjects, 8 non-insulin-dependent diabetic patients, and 5 nondiabetic patients with autoimmune diseases. Beta-cell inhibition by IDDM sera was not observed when complement was omitted. After serum fractionation, the cytotoxic potency of IDDM sera was located in the immunoglobulin G fraction. Using human islets, insulin release was suppressed by 3 of 6 IDDM sera. Complement-dependent cytotoxicity was found in 1 of 5 recent-onset IDDM patients and 11 of 16 IDDM patients with autoimmune phenomena. It was associated in all cases with the presence of islet cell antibodies as detected by immunofluorescence, and with the presence of circulating lymphocytes which suppressed insulin release in vitro. Complement-fixing antibodies may contribute to the selective beta-cell damage in IDDM.

Adolescent↗
PubMed1981

[Substitutes for the endocrine pancreas].

Since it is generally accepted that a tight metabolic control might prevent the chronic complications of diabetes mellitus, several systems have been developed in which insulin is administered in a manner that mimicks the characteristics of insulin secretion. 1) In the so-called closed-loop systems, insulin delivery is regulated by the concomitant plasma glucose level. These systems, which involve continuous measurement of plasma glucose concentration are not to date implantable and have been used so far only for short-term studies. 2) By contrast, in the "open-loop systems", no glucose sensor is needed and insulin delivery is pre-programmed to achieve a constant basal infusion with peaks of insulin delivery during the meal periods. These systems have been used in man for several months. The present achievement and limitations of both kinds of systems are discussed in this review.

Diabetes Mellitus↗
PubMed1981

Minor haemoglobin fractions in uraemic and in diabetic patients.

Using a high resolution automated chromatographic method, the levels of the different minor haemoglobins Hb A1a, A1b, and A1c were measured in 20 healthy controls, in 20 patients with chronic renal failure, in 20 uraemic patients on intermittent haemodialysis, and in 20 insulin-dependent diabetic patients. In uraemic non haemodialysed patients, the levels of the three minor fractions were increased significantly. The two fractions Hb A1b and A1c were normalised subsequent to haemodialysis, whereas the level of Hb A1a was higher in the haemodialysed than in the uraemic non haemodialysed group. In both groups of uraemic patients, no correlation was found between the minor Hb fractions and the corresponding serum creatinine, uric acid, urea, phosphorus, bicarbonate and blood glucose levels. In diabetic patients, the three minor fractions were increased. As expected, Hb A1c and glucose concentrations were tightly correlated. No correlation was found between blood glucose levels and Hb A1a, whereas a correlation existed between blood glucose levels and Hb A1b. It is concluded that the increase of minor haemoglobin fractions in renal failure does not only reflect the glucose intolerance. Renal failure itself causes an increase of the three minor fractions. Overall assay of the minor haemoglobin components (Hb A1) may lead to misinterpretation in case of diabetic patients with chronic renal failure.

Adult↗