PubMed Health⌕ Search

Biomedical subjects

E F Pfeiffer

Publications and source records attributed to E F Pfeiffer.

At least 109 records · Page 6Linked to original sources
PubMed1987

Autoantibodies to pituitary corticotropin-producing cells: possible marker for unfavourable outcome after pituitary microsurgery for Cushing's disease.

Circulating autoantibodies to human fetal pituitary cells were detected in 13 out of 51 patients who underwent transsphenoidal microsurgery for Cushing's disease. The absence of Fc receptors on human fetal pituitary corticotropin-producing cells allowed the detection of antibodies to these cells. In all the 13 patients, the antibodies were present before surgery, and 10 of them showed clinical and/or biochemical signs of incomplete cure of Cushing's disease after surgery. Only 3 out of 27 patients with a favourable outcome were antibody-positive. In all the antibody-positive patients, the antibodies were directed to corticotropin-producing cells and in 8 patients also to luteinising hormone or human growth hormone producing cells. A non-antigen-specific adherence of antibodies to Fc-receptors on corticotropin-cells was excluded by unchanged binding after preincubation of sections with purified rabbit Fc or Fc aggregates. The presence of pituitary corticotropin-cell antibodies in patients with Cushing's disease is associated with an unsuccessful outcome after transsphenoidal selective adenectomy.

Adenoma↗
PubMed1987

[Distribution of adipose tissue and complications of obesity in overweight women with and without hirsutism].

A correlation between the serum androgen levels and the distribution pattern of adipose tissue as well as occurrence of complications of obesity were investigated in 24 obese women with and without hirsutism. The hirsute women (n = 12) displayed higher androgen levels than the women without hirsutism (n = 12) of the same age and weight and possessed a more abdominally pronounced distribution of adipose tissue measured as the quotient of waist and hip circumference (0.87 +/- 0.08 as compared to 0.76 +/- 0.06; P less than 0.05). In addition, the overweight women with hirsutism had higher fasting triglyceride levels as well as higher values of systolic and diastolic blood pressure. Overall, a positive correlation was found between testosterone and the ratio of waist and hip circumference (r = 0.40; P less than 0.05) and the values of diastolic blood pressure (r = 0.51; P less than 0.01). Moreover, the ratio of waist and hip circumference correlated with the systolic blood pressure values (r = 0.61; P less than 0.001), the fasting triglyceride levels (r = 0.42; P less than 0.05) as well as the basal insulin concentration (r = 0.48; P less than 0.05). These results are an indication that raised androgens predispose to accumulation of fat in the abdominal region. In turn, an android distribution of adipose tissue is associated with more frequent metabolic disorders and vascular hypertension.

Adipose Tissue↗
PubMed1987

On the way to the automated (blood) glucose regulation in diabetes: the dark past, the grey present and the rosy future. XII Congress of the International Diabetes Federation, Madrid, 22-28 September 1985.

The development of the artificial pancreas represents an important step forward in modern diabetology. The practical and theoretical findings obtained by its application to Type 1 (insulin-dependent) diabetic patients has given new insights into modes of insulin secretion, pathophysiology of diabetes mellitus, and new forms of treatment, i.e. the development of portable insulin pumps and intensified conventional insulin therapy. All of these therapies provided better results than conventional insulin administration. However, there is no doubt that the restoration of normoglycaemia in a real sense is obtainable only by an implantable artificial pancreas or pancreas transplantation. The development of the implantable artificial pancreas, on the other hand, is dependent upon the development of a reliably working permanently implantable glucose sensor. The first attempts in that direction have opened new vistas as to the differences between blood and interstitial tissue glucose measurements, displaying different modes of regulation under normal and pathologic conditions. A number of barriers have to be overcome until the final goal has been attained: to obtain, by automated blood glucose control, narrow glycaemic fluctuations of the normal subject, and to prevent, hopefully, relentless diabetic complications.

Animals↗
PubMed1987

The effect of artificial sweetener on insulin secretion. 1. The effect of acesulfame K on insulin secretion in the rat (studies in vivo).

Acesulfame K is an artificial sweetener which has been used in the food industry for some years. As yet no metabolic effects have been reported. It was reported that the sweetener can induce a cephalic phase of insulin secretion. To analyse the mechanism of this phenomenon, we studied the effect of Acesulfame K on insulin secretion in vivo. Male Wistar rats, weighing 250-300 g were fasted overnight and anaesthetized with phenobarbital. A silicon catheter was inserted into the right cervical vein for injection of test substances and for obtaining blood samples. In some experiments, another catheter was inserted into the left cervical vein for continuous infusion. Blood samples were drawn at 0, 5, 10, 15, 30 and 60 min after injection, and at -10, 0, 10, 20, 30, 40, 60, 80, 100 and 120 min after the infusion started. Injection of Acesulfame K (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3 +/- 3.0 microU/ml to 58.6 +/- 4.2 microU/ml without any significant change in the blood glucose. Infusion of Acesulfame K (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 microU/ml) during this period, and at the same time blood glucose was gradually reduced from 103.0 +/- 7.3 to 72.0 +/- 7.2 mg/dl. When using different amounts of Acesulfame K, the insulin secretion was stimulated in a dose-dependent fashion. The effect of Acesulfame K on insulin secretion was similar to that observed by injecting or infusing the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effect of artificial sweetener on insulin secretion. II. Stimulation of insulin release from isolated rat islets by Acesulfame K (in vitro experiments).

The effect of the artificial sweetener Acesulfame K on insulin release in vitro was investigated. Pancreatic islets were obtained from Male Wistar rats. Acesulfame K produced a significant increase in insulin release from incubated islets. This effect was dose- and glucose-dependent. When islets were incubated with different amounts of Acesulfame K (2.5, 7.5 and 15 mM) and 15 mM glucose in the media for one hour, insulin concentrations were 140.2 +/- 21.1, 246.7 +/- 32.4 and 313.9 +/- 37.7 microU/ml, respectively. When 15 mM Acesulfame K was added to a media containing 0, 2.5, 5, 10 and 15 mM glucose, insulin release from incubated islets after 60 min were 25.6 +/- 6.4, 65.4 +/- 12.1, 109.0 +/- 10.0, 229.6 +/- 28.0 and 313.9 +/- 37.7 microU/ml. Incubating islets in the media containing arginine or acetylcholine increased insulin release significantly. However, when Acesulfame K was added to the media containing either arginine or acetylcholine, no further potentiating effect could be detected. The effect of Acesulfame K on insulin secretion was decreased by noradrenaline. However, the addition of naloxone, atropine and propranolol had no significant effect. Somatostatin inhibited insulin release from isolated pancreatic islets, but did not antagonize the action of Acesulfame K. When 2.5 mM Acesulfame K was added to a medium containing somatostatin, the inhibitory effect of somatostatin was totally neutralized. In a perifusion system, Acesulfame K stimulated both phases of insulin secretion. In conclusion, Acesulfame K acts directly on the pancreatic islets and potentiates glucose-induced insulin release.

Animals↗
PubMed1987

Further evidence that prolactin does not affect gonadotropin release at pituitary level.

In a primary monolayer cell culture of the anterior pituitary from mature male rats the effects of exogenous rPrl (rPrl exog.) and endogenously secreted rPrl (rPrl endog.) on basal and LHRH stimulated LH secretion were investigated. In pilot studies basal Prl- and LH secretion as well as influence of various LHRH concentrations (10(-1)-10(+3) ng/ml) on Prl- and LH release were observed. The influence of exogenous rPrl was studied at various concentrations (50-500 ng/ml) and with preincubation periods of 2 hrs and 6 hrs before starting LHRH stimulation. The dopamine agonist bromocriptine and the dopamine antagonist sulpirid were preferentially used to prove physiologic function of the cell system presented. Basal LH secretion started after a delay of 3 hrs, whereas basal Prl secretion began immediately showing a linear rise for 9 hrs. LHRH stimulation resulted in a non-linear dose and time dependent LH secretion. LHRH showed no influence on endogenous Prl (rPrl endog.) secretion of the mammotroph cells. Exogenous Prl (rPrl exog.) did not affect spontaneous Prl release excluding ultra short loop inhibition in this cell system. Furthermore, exogenous Prl had no effect on either basal or LHRH stimulated LH secretion even after a preincubation period of up to 6 hrs and at concentrations generally observed for prolactin secreting tumors. Bromocriptine suppressed endogenous Prl release and did not affect LH secretion. Sulpirid had no influence on either Prl or LH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Glucocorticoids and insulin promote the differentiation of human adipocyte precursor cells into fat cells.

To study the in vitro differentiation of human adipocyte precursor cells and its regulation by hormones, primary cultures of stromal vascular cells of human adipose tissue were established. A 30- to 70-fold increase in the number of developing fat cells was achieved by the addition of cortisol or related corticosteroids in the presence of insulin. Either of the two hormones alone was ineffective. The stimulatory action of cortisol was dose dependent and occurred at physiological concentrations. The results suggest that glucocorticoids may play a role in the development of human hyperplastic obesity by stimulating the formation of adipocytes from precursor cells.

Adipose Tissue↗