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Biomedical subjects

S Efendic

Publications and source records attributed to S Efendic.

At least 181 records · Page 10Linked to original sources
PubMed1985

Effect of improved glycemic control by continuous subcutaneous insulin infusion on hormonal responses to insulin-induced hypoglycemia in type 1 diabetics.

Glucose counter-regulatory capacity and the hormonal responses to insulin-induced hypoglycemia were studied in eight type 1 diabetics before and after improvement of metabolic control by continuous subcutaneous insulin infusion (CSII). The intensified treatment resulted in a decrease in mean glycosylated hemoglobin from 11.6 +/- 0.5 to 9.3 +/- 0.4% within a mean period of 14 weeks. During a constant rate infusion of insulin (2.4 U/h), steady state levels of glucose appeared in all subjects. The steady state glucose level was identical before and after CSII. The counter-regulatory hormonal responses showed significantly higher epinephrine levels, while glucagon, growth hormone, and cortisol were not influenced. In parallel with the heightened epinephrine response the pulse rate response was significantly enhanced. The restitution of blood glucose after insulin hypoglycemia was not modified. It is concluded that a more vigorous catecholaminergic response to hypoglycemia is achieved after improved metabolic control by CSII.

Adult↗
PubMed1984

Impaired counter regulation of hypoglycemia in a group of insulin-dependent diabetics with recurrent episodes of severe hypoglycemia.

The counterregulatory response to insulin-induced hypoglycemia was investigated in 22 insulin-dependent diabetics (IDD) with recurrent hypoglycemia and in 6 healthy volunteers. Hypoglycemia was induced by a constant rate infusion of insulin (2.4 U/h) up to four hours. Conventional insulin therapy was changed to an i.v. infusion of regular insulin 24 hours prior to the experiment. The presence of diabetic autonomic neuropathy was evaluated by respiratory sinus arrhythmia and Valsalva maneuver. In healthy subjects, blood glucose was decreased to 2.5 mmol, here reaching steady state level and giving rise to marked glucagon and growth hormone (GH) responses. The majority of IDD (group A) reached a slightly lower steady state glucose level and exhibited similar glucagon and GH responses while the epinephrine response was augmented. Six IDD (group B) showed a continuous decrease in blood glucose to 1.2 +/- 0.1 mmol/l at which level the infusion of insulin was discontinued due to neuroglucopenic symptoms. These subjects had no glucagon and epinephrine responses while their GH and cortisol responses were normal. A comparison of the diabetic groups revealed a longer duration of diabetes and a more impaired autonomic nervous function in group B while glycosylated hemoglobin was similar. It is concluded that most IDD have normal hormonal responses (epinephrine, glucagon, GH, cortisol) and normal counterregulartory capacity to hypoglycemia induced by a prolonged infusion of a moderate dose of insulin. Some patients with long-term diabetes and impaired capacity to counteract hypoglycemia exhibit deficient glucagon and epinephrine responses to hypoglycemia.

Adult↗
PubMed1982

Effect of somatostatin on insulin-induced hypoglycemia in man.

In order to study the interaction of insulin and somatostatin on glucose regulation in the posthypoglycemic phase of a somatostatin infusion we have applied a bolus of i.v. insulin to healthy subjects receiving a continuous infusion of somatostatin. Glucose, insulin and counterregulatory hormones were determined. Somatostatin suppressed the growth hormone and glucagon responses to hypoglycemia but did not augment the hypoglycemic action of insulin. In contrast, the K-value for the decrease in blood glucose was significantly lower in the presence of somatostatin. Thus, the interaction of insulin and somatostatin on glucose metabolism is complex and time-dependent. While the peptide potentiates the action of insulin during the first hour of somatostatin infusion, it counteracts if after two hours. As somatostatin has currently been introduced in the therapy of upper gastrointestinal bleedings, these effects of the peptide must be taken into consideration.

Adult↗
PubMed1982

Glucose, insulin and osmolality changes in rats sustaining different hemorrhage volumes.

Plasma glucose, osmolality and insulin have been investigated during hemorrhage in non-starved rats. The rate of blood loss leading to hemorrhages of 44% and 55% of the estimated original blood volume determined the patterns of response. Substantial hyperglycemic hyperosmolality and insulin values appropriate for the raised levels of glucose were observed in the animals bleeding more rapidly. The slower rate of hemorrhage was associated with only moderate hyperglycemia and hyperosmolality, while the insulin values rose to very high levels, 45 times basal. It is postulated that altered glucose-insulin metabolism in haemorrhage may have important consequences for fluid homeostasis, and the rate of bleeding is the fundamental factor steering this effect.

Animals↗
PubMed1981

Effects of graded doses of somatostatin on gallbladder emptying and pancreatic enzyme output after oral glucose in man.

Effects of intravenous somatostatin on the secretion, motility and absorption in the upper gastrointestinal tract after 75 g oral glucose were examined in healthy subjects with a quantitative multiple indicator dilution method. This report deals with the effects on the gallbladder emptying and the pancreatic enzyme output. Intake of a hypertonic glucose solution induces rapid gallbladder emptying. After early peaks, both biliary and pancreatic enzyme outputs remain at a steady lower level to the end. Somatostatin, started 20 min before the oral load, inhibited dose-dependently the gallbladder emptying and pancreatic enzyme secretion. A maximal inhibition was attained by 1.5 microgram . min-1, and 0.05 microgram . min-1 somatostatin gave a significant 40% reduction. The inhibition persisted in the postinfusion period and was followed by delayed rebound outputs. The gallbladder emptying was completely arrested for variable periods of time, but the pancreatic enzyme secretion was never totally blocked. The promptly established arrest of the gallbladder differed from the slowly initiated inhibition of the gastric and intestinal propulsion. It is proposed that the multiple ways of action of somatostatin and different stimulatory levels contribute to the discrepancies. The study shows that somatostatin induces dose-dependent, long-lasting inhibitions of the biliary and pancreatic responses to oral glucose. The minimal effective dose was a hundred times lower than the dose tested in previous studies in man.

Administration, Oral↗
PubMed1981

Dosage of insulin during delivery and the immediate post-partum period in pregnant diabetics.

Several different principles have been presented for treatment of the pregnant diabetic in connection with labor. There is, however, a lack of documentation of blood glucose levels in the immediate post-partum period. On the day of delivery and on the 2 following days, 55 diabetics were given one daily injection of an intermediate-acting insulin, irrespective of the mode of delivery. The amount of insulin given was one-third of the total dose on the day before delivery. From 07.00 hours on the day of delivery, blood-glucose levels were determined every fourth hour for 48 hours. This insulin dosage gave a satisfactory control of glycemia with a low incidence of hypoglycemia and additional insulin was very seldom required.

Adolescent↗
PubMed1980

Decreased release of somatostatin into the portal vein following electrical vagal stimulation in the cat.

Electrical vagal stimulations were performed in anesthetized cats, in which the spleen and the intestine below the duodenum had been removed. The cats were provided with acute antral pouches which were perfused during the experiments. Insulin, glucagon, gastrin and somatostatin were measured in portal vein blood (consisting of blood from the stomach and the pancreas). The antral perfusates were analyzed for gastrin and somatostatin. Electrical vagal stimulation increased the release of insulin and glucagon into the portal vein. Gastrin was elevated in antral perfusates and portal vein blood, whereas somatostatin increased the antral perfusates, but was reduced in portal vein blood. We assume that antral somatotostatin, like gastrin, is released into the blood. The finding that portal vein somatostatin was decreased following vagal stimulation, indicates that the release of somatostatin from another large source of somatostatin, presumably the fundic region of the stomach or the pancreas, was decreased by vagal activation.

Animals↗
PubMed1980

Effect of intraluminal pH on the release of somatostatin and gastrin into antral, bulbar and ileal pouches of conscious dogs.

Experiments were performed on conscious dogs with chronic pouches of the antrum, the duodenal bulb or the ileum, which were perfused with solutions of varying pH. Gastrin and somatostatin levels were measured in the perfusates. When the pouches were perfused with 0.15 M NaCl only small amounts of gastrin and somatostatin (1 pmol/min) were released into the lumen of the antrum and of the duodenal bulb. By lowering pH of the perfusion fluid a pH dependent release of somatostatin was induced into the lumen of the antrum and the duodenal bulb. Perfusion with 0.1 M HCl caused a large output of somatostatin (6--60 pmol/min) into the pouches. The upper pH limit for stimulation of the intraantral or intrabulbar somatostatin release appeared to be approximately pH 3--4. Somatostatin was also released into ileal perfusates at intraluminal pHs below 3--4. Lowering of pH in the antral pouches caused an increased intraluminal gastrin release, which was quantitatively less impressive than that of somatostatin. Occasionally also the gastrin release into the duodenal bulb increased during perfusion with 0.1 M HCl, whereas no such release was induced by acidification of the lumen of the ileum. It is suggested that the inhibition of gastrin release observed at low intraantral pH is mediated by a local effect of somatostatin, since this peptide is released in a pH dependent manner in the antropyloric region. It is also suggested that acidification of any region of the gastrointestinal tract will stimulate the release of peptides from all endocrine cells of the open type, probably by an unspecific effect on the membrane. Thus both gastrin and somatostatin are released by acidification of the antrum, but in the presence of high local levels of somatostatin, the release of gastrin is substantially inhibited.

Animals↗
PubMed1979

Release of gastrin from the skeletal muscles and from the antral mucosa in cats induced by sulfonuric drugs.

The present observations indicate that sulfonuric drugs release gastrin both from peripheral nerves in striated muscles and from endocrine-like cells in the gastrointestinal tract. Gastrin appears in perfusates of extirpated cat legs after administration of tolbutamide or glibenclamide (5-50 mg/kg or 5-500 microgram/kg perfused tissue respectively) to the perfusion medium. Furthermore gastrin is released into the portal vein of cats after i.v. administration of glibenclamide (5-50 microgram/kg). The finding that sulfonuric drugs not only release insulin from beta-cells in the pancreas, but also gastrin from gastrin producing cells in the stomach as well as from nerve fibers in the skeletal muscles, indicate that sulfonuric drugs have more wide spread effects than previously assumed. Possible consequences of the drug induced release of peptides from peripheral nerves as well as of the release of gastrin from the gastrointestinal tract are discussed.

Animals↗
PubMed1979

Effect of two sulphonylureas on the dose kinetics of glucose-induced insulin release in normal and diabetic subjects.

The effect of two second generation sulphonylureas, gliquidone and glibenclamide, on insulin secretion has been studied in the basal state and in combination with glucose infusions in normal controls, patients with mild maturity-onset diabetes, and subjects with normal glucose tolerance but low insulin response. When injected intravenously, gliquidone caused rapid elevation of plasma insulin, peaking at 5 min in all groups, while glibenclamide induced a slow rise in insulin. Insulin response was somewhat smaller than normal in diabetics and low insulin responders. In all groups, 25 micrograms/kg glibenclamide and 200 micrograms/kg gliquidone were equipotent in generating an insulin response at the basal state. Equipotent amounts of sulphonylureas were combined with glucose in fusions at three different dose levels. The glucose-insulin dose relationships, established by giving glucose alone, demonstrated curves that were flatter, and shifted to the right of the control in diabetics and low insulin responders, the changes being more marked in the former group. Addition of sulphonylurea induced a left shift in the dose-response relationships in controls and low insulin responders; under these conditions the effect of glibenclamide was more pronounced than that of gliquidone. The dose-response relation for glucose-induced insulin release was completely normalized in low responders when sulphonylureas were added. In the group of mild diabetics, insulin response to glucose was enhanced by sulphonylureas only to a modest extent, the dose-response curves remaining grossly abnormal.

Adult↗
PubMed1979

Phosphate buffer stimulates somatostatin release into the antral lumen of anaesthetized cats.

The effect of variations of intra-antral pH on the intraluminal release of somatostatin was studied. Acute pouches were created in anaesthetized cats, and the pouches were perfused with solutions differing in pH. Somatostatin levels were then measured in the perfusates. In this model phosphate buffer was a potent stimulator of intra-antral somatostatin release, whereas perfusion with 0.1 M HCl failed to release somatostatin by itself. Since phosphate buffer also releases gastrin, the releasing effect ought to be exerted beyond the mechanism that can be blocked by somatostatin. (Thus the stimulatory effect of phosphate buffer might be exerted on the membranes of the endocrine cells.)

Animals↗