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Biomedical subjects

E F Pfeiffer

Publications and source records attributed to E F Pfeiffer.

At least 271 records · Page 15Linked to original sources
PubMed1975

Effect of lipids on insulin, growth hormone and exocrine pancreatic secretion in man.

Influences of fat on release of insulin, growth hormone and pancreatic enzyme secretion were studied in 35 metabolically healthy subjects. A fat solution containing 40 g of soy bean oil was administered, I.V., orally and intraduodenally. In all cases there was a similar increase of insulin but the rise in serum insulin after oral or intraduodenal fat administration was not related to the changes in plasma free fatty acids, free glycerol and triglyceride levels. Blood surgar responded according to insulin secretion. The route of fat administration may possibly influence growth hormone secretion. Following intraduodenal fat administration volume and bicarbonate contents of the duodenal juice rose slightly whereas trypsin and bilirubin content increased considerably. These results suggest that insulin secretion after oral or intraduodenal administration of fat is influenced by intestinal factors. Cholecystokinin-pancroezymin and gastric inhibitory polypeptide are qualified to serve as such factors.

Blood Glucose↗
PubMed1975

[Continuous daily blood-sugar profile in relation to serum insulin in subjects with normal metabolism and ideal or normal weight (author's transl)].

Continuous blood-sugar measurement is at present the most suitable method for testing daily blood sugar profile. It allows to relate variations in blood sugar levels in metabolically normal subjects to body weight. Mean blood-sugar level and postprandial blood-sugar variations are greater in those of normal than of ideal weight. At the same time, metabolically normal subjects of normal weight have a high insulin secretion in the fasting and postprandial states. This makes it likely that those of normal weight, although it is only slightly different from those of ideal weight, have already reached a transitional stage to an increased diabetes risk from over-weight.

Blood Glucose↗
PubMed1975

Insulin secretion in the perinatal period of the rat in vivo and in vitro effects of glucose and gibenclamide (HB 419).

During the perinatal period of the rat the effect of glucose and glibenclamide (HB 419) on the secretion of insulin was studied in vivo and in vitro. In the in vitro experiments isolated islets of 21 day old fetal and 5 day old newborn rats were perifused wtih 16.7 mM glucose or 16.7 mM glucose plus 1 mug/ml glibenclamide, while in the in vivo ecperiments glucose, 0.5 g/kg of body weight, or glibenclamide, 0.5 mg/kg of body weight were tested. Glucose elicited a small first phase of insulin release in 21 days old fetal islets, while glucose plus glibenclamide evoked a biphasic pattern. The injection of glibenclamide to the mother lowered the blood sugar in the fetus and increased the fetal serum insulin concentration. In one day old newborn rats glibenclamide stimulated the secretion of insulin after an i.p. injection. Glucose was without effect. Both substances increaseded the serum insulin concentration in five day old newborn animals. Dynamic studies at that age revealed a monophasic response to glucose and a biphasic pattern to glucose plus glibenclamide.

Animals↗
PubMed1975

Somatostatin-induced inhibition of insulin secretion from isolated islets of rat pancreas in presence of glucagon.

In order to study the oeffect of somatostatin on the endocrine pancreas directly, islets isolated from rat pancreas by collagenase were incubated for 2 hrs 1) at 50 and 200 mg/100 ml glucose in the absence and presence of somatostatin (1, 10 and 100 mg/ml) and2) at 200 mg/100 ml glucose together with glucagon (5 mug/ml), with or without somatostatin (100 ng/ml). Immunologically measurable insulin was determined in the incubation media at 0, 1 and 2 hrs. Insulin release was not statistically affected by any concentration stomatostatin. On the other hand, somatostatin exerted a significant inhibitory action on glucagon-potentiated insulin secretion (mean +/- SEM, mu1/2 hrs/10 islets: glucose and glucagon: 1253 +/- 92; glucose, glucagon and somatostatin: 786 +/- 76). The insulin output in th epresence of glucose, glucagon and somatostatin was also significantly smaller than in thepresence of glucose alone (1104 +/- 126) or of glucose and somatostatin (1061 +/- 122). The failure of somatostatin to affect glucose-stimulated release of insulin from isolated islets contrasts its inhibitory action on insulin secretion as observed in the isolated perfused pancreas and in vivo. This discrepancy might be ascribed to the isolation procedure using collagenase. However, somatostatin inhibited glucagon-potentiated insulin secretion in isolated islets which resulted in even lower insulin levels than obtained in the parallel experiments without glucagon. It is concluded that the hormone of the alpha cells, or the cyclic AMP system, might play a part in the machanism of somatostatin-induced inhibition of insulin release from the beta-cell.

Animals↗
PubMed1975

Effects of somatostatin on gastric secretion and gastrin release in man.

Somatostatin, a recently synthesized hypothalamic growth hormone release-inhibiting factor (GIF), was used in the cyclic and linear form. In all subjects studied, the cyclic GIF inhibited gastrin secretion during basal conditions as well as during a standard food stimulus, with immediate rebound after the infusion was stopped. Similar responses were observed in a hypophysectomized patient, indicating that this effect of GIF was independent of suppression of growth hormone secretion. Cyclic and linear GIF, when administered in normal subjects during an infusion of synthetic human gastrin I, almost totally suppressed gastric secretion. The results indicate that GIF is a potent inhibitor of gastric secretion and gastrin release.

Gastric Juice↗
PubMed1975

Chromatographic heterogeneity of insulin extracted from insulomas.

On gel filtration of acid-ethanol extracts from three pancreatic beta-cell adenomas 1.4% to 1.8% of total immunomeasurable insulin (IMI) eluted ahead of proinsulin. This high molecular IMI was resolved into three components. The presence of urea in the dilute acetic acid solutions of extracted tumor tissue did not influence the pattern of gel filtration. High molecular IMI dissolved in dilute acetic acid showed to be stable if immediately rechromatographed, but a partial dissociation to insulinlike and proinsulinlike components (ILC and PLC) was found if rechromatography was performed after 48 h of incubation. Mainly ILC and PLC were found on rechromatography provided high molecular IMI was dissolved and incubated briefly in 0.04M phosphate buffer, pH 7.4. It proved improbable that the proteolytic action of some protein being extracted with the hormones caused a splitting of high molecular IMI at pH 7.4. We conclude from our findings that the components of high molecular IMI are not precursors of proinsulin and insulin but are either self-associated products of the hormones or associations of insulin and proinsulin to other proteins extracted from insuloma tissue.

Adenoma, Islet Cell↗
PubMed1975

Immunological relatedness of human and porcine growth hormones.

The immunological relatedness of human and porcine growth hormones is examined by means of labelled human growth hormone and guinea pig antiserum. 1) Labelled human growth hormone is found in the precipitate after reaction with antiserum against porcine growth hormone. Parallel dilution curves are obtained with antisera against human and porcine growth hormones. 2) After addition of antiserum against porcine growth hormone, all the radioactivity is eluted from Sephadex G-100 with the void volume. 3) The addition of an excess of porcine hormone displaces labelled human growth hormone from antibodies against human growth hormone to the same extent as an excess of non-labelled human growth hormone does. 4) The standard radioimmunoprecipitation curves for porcine and human growth hormones obtained in the assay system for the human hormone are parallel in slope, provided that the human hormone and our preparation of the porcine hormone are introduced at a proportion of 1 to 560. 5) In a double diffusion test in agarose gel layers, with human and porcine growth hormones diffusing against guinea pig anti-porcine serum, cross reaction is observed. The conclusion is drawn that with guinea pig antisera, human and porcine growth hormones behave immunologically in a similar fashion. Labelled human growth hormone seems to have only such immunodeterminants as are also found in porcine growth hormone.

Animals↗
PubMed1975

Immunological identity of human and porcine growth hormones. Application to determination of growth hormone in porcine serum.

In two radioimmunoassay systems with iodinated human growth hormone as tracer and anti-human growth hormone or anti-porcine growth hormone as binding site, the standard curves for human and for porcine growth hormone were parallel. In both systems the porcine growth hormone preparation had to be added in about the same excess as compared to the human hormone. It was concluded that the human and the porcine hormones behave in an identical way and that the values obtained in radioimmunoassay for human growth hormone represent the amount of immunologically active molecules in the porcine growth hormone preparation. As parallel standard curves were obtained with porcine serum, the concentration of growth hormone is porcine serum may be determined by radioimmunoassay for human growth hormone.

Animals↗
PubMed1975

Interactions of concanavalin A with isolated pancreatic islets.

Pancreatic islets of mice were isolated by the collagenase method. After a preincubation period of 20 min they were incubated in Krebs-Ringer-albumin buffer in the presence of glucose. Concanavalin A (2 mg/ml) inhibits the glucose-induced release of insulin; this same property is shown by Concanavalin A bound to nonphagocytosable beads of Sephrose at lower concentrations (0.4 mg/ml). In pancreatic islets stimulated by tolbutamide, glibenclamide or arginine the secretion of insulin is not inhibited in the presence of Concanavalin A. The incorporation of tritiated leucine is not influenced by Concanavalin A. Since desialized pancreatic islets react in the same way the glucose-induced secretion of insulin appears to be a membrane-dependent process.

Animals↗
PubMed1975

Dissociation of in vivo and in vitro "autonomy" in human adrenocortical tumour.

The diagnosis of Cushing's syndrome due to "autonomous adrenocortical tumour" has been established in a patient by appropriate examinations (especially dexamethasone suppression test, ACTH stimulation test, ACTH measurement by radioimmunoassay). Isolated cells have been prepared from a piece of the tumour by a trypsin technique so that the action of ACTH on steriodogenesis in these cells could be studied in vitro. Basal production of corticosteroids by the isolated tumour cells was low (0.3 mu plus or minus 0.04/2 h/10-5 cells). Addition of ACTH induced a dose-dependent stimulation of corticosteroid production. The tumour cells appeared to be unable to produce corticosteroids in the absence of ACTH; maximal production was rather low (1.38 mu plus or minus 0.07/2 h/10-5 cells). A possible explanation for the discrepancies between endocrine function tests and the results of the in vitro studies is given.

Adrenal Cortex Hormones↗
PubMed1975

Growth in monolayer culture of rat pituitary cells which synthetize and release acth.

Cultures of rat pituitary gland cells were developed to study biosynthesis and release of ACTH. ACTH measurement was accomplished by radioimmunoassay. ACTH release was observed following stimulation with theophylline and cAMP in a dose-dependent manner. Biosynthesis was demonstrated by incorporation of 3-H-phenylalanine into the hormone, employing a double antibody technique.

Adrenocorticotropic Hormone↗
PubMed1975

Antidiabetic action of somatostatin--assessed by the artificial pancreas.

By means of a glucose-controlled insulin- and glucose-infusion system (GCIGIS) we examined the effect of somatostatin on insulin and glucose requirements following meals or oral glucose loads in juvenile diabetics. In six of seven patients the insulin requirement with somatostatin was remarkably reduced to between 38 per cent and 79 per cent of that of otherwise identical control experiments. No reduction could be found in the seventh case, fed only 575 kcal. In all cases we observed an increase in dextrose demanded from the GCIGIS ranging between 28 per cent and 192 per cent of the control amounts. In addition, a lowering and smoothing of postprandial blood glucose curves caused by somatostatin application was a general finding. It seems to us most likely that the well-known suppression of the secretion of growth hormone and glucagon, both insulin antagonists, is responsible for the antidiabetic action of somatostatin.

Adolescent↗
PubMed1975

Insulin biosynthesis in isolated pancreatic islets of fetal and newborn rats.

The effect of glucose and glucose plus glucagon on the incorporation of H-3-L-leucine into proinsulin and insulin was examined in isolated islets of twenty-one-day old fetal and five- and ten-day old newborn rats. Maximal stimulation of (pro-) insulin biosynthesis was achieved with 100 mg. per cent of glucose in isolated islets of twenty-one-day old fetal rats. No additional effect was observed with 300 mg. per cent of glucose. On the other hand, in islets of five- and ten-day old newborn rats the incorporation of H-3-L-leucine into proinsulin and insulin was gradually augmented by glucose up to concentrations of 300 mg. per cent. Addition of glucagon to the various glucose concentrations only enhanced the synthesis of insulin in ten-day old newborn islets, whereas it had no effect on the islets of the younger age groups. The results show a different pattern of insulin biosyntheses in fetal and newborn islets, which may be related to the varied plasma glucose concentrations of the perinatal period.

Age Factors↗