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Biomedical subjects

J Mössner

Publications and source records attributed to J Mössner.

At least 181 records · Page 10Linked to original sources
PubMed1986

Intestinal absorption of folic acid, glucose, sodium and water in chronic pancreatitis.

Intestinal absorption of folic acid, glucose, water and sodium in 10 patients with chronic pancreatitis who have abstained from alcohol for at least 2 months is compared with 18 agematched outpatients without gastrointestinal disorders and a daily alcohol intake less than 30 g. Intestinal absorption was measured by segmental perfusion of the jejunum using a triple lumen tube. Patients with chronic pancreatitis showed a significantly decreased absorption of folic acid and glucose, whereas the net absorption of water and sodium was not disturbed.

Adult↗
PubMed1985

Insulin, via its own receptor, regulates growth and amylase synthesis in pancreatic acinar AR42J cells.

Previous in vivo studies have suggested a long-term regulatory role for insulin in the exocrine pancreas. To directly study the long-term effects of insulin on the pancreas in vitro, we have used cultured AR42J cells, a rat cell line that is derived from a transplantable tumor of the acinar pancreas. Hormone-binding experiments with 125I-labeled hormones indicated that AR42J cells have insulin receptors, relatively fewer receptors for insulin-like growth factor II (IGF-II), and no detectable receptors for insulin-like growth factor I (IGF-I). Insulin at concentrations as low as 1 nM stimulated the growth of these cells, as measured by an increase in DNA and protein content, and in cell number. At 100 nM, where insulin had a maximal effect, the growth of AR42J cells was stimulated by 46.1 +/- 10.9% (mean +/- SEM, N = 11). Insulin increased the amylase activity of AR42J cells over the same concentration range that it stimulated growth; at 100 nM, insulin increased amylase by 91.0 +/- 15.4% (mean +/- SEM, N = 23). Immunoprecipitation of [35S]methionine-labeled proteins revealed that insulin induced a selective increase of amylase synthesis over general protein synthesis. These studies indicate, therefore, that insulin stimulates both growth and amylase synthesis of AR42J cells.

Amylases↗
PubMed1985

[Insulin--a regulator of exocrine pancreas function?].

The following is a review of the literature concerning experimental data on insulin effects in the exocrine pancreas and a discussion whether those experimental data give prove to an important role of insulin in the regulation of the exocrine pancreatic function. Morphological features of an endocrine/exocrine relationship like a special vascularisation and periinsular "halos", a hypertrophy of acini adjacent to the islets of Langerhans, are described. Next the characteristics of the insulin receptor of exocrine pancreatic acini and its regulation by insulin, so called "up- and downregulation", are discussed. This is followed by a description of the exocrine pancreatic function in type I diabetes of humans and in experimental insulin deficiency diabetes of rats. Short term effects of insulin on the exocrine pancreas in vitro, using isolated pancreatic acini, like stimulation of glucose- and aminoacid uptake, stimulation of proteinsynthesis, phosphorylation of certain proteins and stimulation of CCK induced amylase release are discussed. Next potential long term effects of insulin on the exocrine pancreas in vivo like regulation of the synthesis of certain digestive enzymes are described, followed by a discussion of long term insulin effects in vitro employing AR42J cells, a rat pancreatic carcinoma acinar in origin. Additionally the insulin like growth factors and their unknown role in the exocrine pancreas are mentioned.

Animals↗
PubMed1984

Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin.

Previously, we reported that pancreatic acini have specific receptors for the insulin-like growth factors (IGF) I and II. We now report that the binding of 125I-labeled IGF II to mouse pancreatic acini is maximally increased by 100 nM insulin (51%) and is maximally reduced by 10 nM cholecystokinin octapeptide (CCK8) (34%), but is not affected by other regulatory peptides such as somatostatin or glucagon. Since many polypeptide hormones are internalized, we determined whether this regulation of IGF II binding occurred via a change in internalization. Acid washing or trypsinization has been shown to remove surface-bound hormone while the acid- or trypsin-resistant radioactivity represents internalized radioligand. Insulin increased and CCK8 decreased the internalization of IGF II as determined by these techniques. Studies of IGF II binding to acini at low temperature (15 degrees C) and binding to particulate fractions from acini were also consistent with the effect of insulin to increase and CCK8 to decrease the internalization of IGF II. When insulin and CCK8 were added together, the inhibitory effect of CCK8 predominated, indicating that CCK8 acted distal to the effect of insulin. Several lines of evidence suggest that this effect of CCK8 was via the CCK receptor and was mediated via a change in intracellular Ca2+: the effect of CCK8 on inhibiting IGF II binding was blocked by the cholecystokinin antagonist N2,O2'-dibutyryl cGMP; the cholinergic agent carbachol (1-100 microM), which acts through the muscarinic receptor to increase intracellular Ca2+, also inhibited IGF II binding; the Ca2+ ionophore A23187 (1-5 microM) mimicked the effects of CCK8 and carbachol. These data indicate, therefore, that CCK8 and possibly insulin may regulate the internalization of IGF II via intracellular Ca2+. Moreover, the data raise the possibility that alterations of hormone internalization may be a general phenomenon of hormone-hormone interaction.

Animals↗
PubMed1984

Cholecystokinin and insulin regulate insulin-like growth factor II binding to pancreatic receptors; evidence of a role for intracellular calcium.

The binding of 125I-labeled insulin-like growth factor II (125I-IGF II) to mouse pancreatic acini was stimulated (45%) by insulin and inhibited (30%) by cholecystokinin octapeptide (CCK8). When CCK8 and insulin were added together, the effect on IGF II binding was similar to that seen when CCK8 was added alone. Two lines of evidence suggest that this effect of cholecystokinin on basal and insulin-stimulated 125I-IGF II binding was mediated via a change in intracellular calcium: (1) the cholinergic agent carbachol inhibited IGF II binding to its receptors; (2) addition of the Ca2+ ionophore A23187 mimicked the effects of CCK8 and carbachol. In contrast to its effects on IGF II binding to acini, CCK8 had only small effects on IGF I binding and no effects on insulin binding.

Animals↗
PubMed1984

Regulation of pancreatic acinar cell insulin receptors by insulin.

In vivo pancreatic acini from normal mice are exposed to very high concentrations of insulin. To determine whether insulin receptors in these acini are downregulated by this endogenous insulin, insulin receptors on acini from both normal and diabetic mice were studied. Isolated acini from normal mice, which have accompanying islets of Langerhans, were studied under conditions where endogenous insulin was minimized. These acini bound 50% less 125I-insulin than acini from mice made diabetic with streptozotocin. Computer analysis of competition-inhibition curves showed a decrease in the number of insulin receptors in acini from normal mice when compared with acini from diabetic mice; however, the IC50 (a measure of receptor affinity) remained unchanged at approximately 1 nM. To study further the regulation of acinar cell insulin receptors, acini from diabetic mice were placed in suspension culture for 24 h. Addition of 1 microM insulin during the culture period led to a 30% decrease in subsequent 125I-insulin binding; the presence or absence of either epidermal growth factor or carbachol was without effect on insulin binding. The decrease in binding induced by insulin resulted from a change in receptor number without an alteration of the IC50. Measurement of total acinar cell insulin receptors by solubilization of these acini in 1% Triton X-100 showed that this insulin-induced decrease was due to a change in the total number of cellular insulin receptors. The present study suggests, therefore, that insulin can regulate its own receptor on pancreatic acini and that in vivo insulin receptors in normal pancreatic cells are downregulated, presumably due to high ambient insulin concentrations.

Animals↗
PubMed1982

[Exocrine pancreas function - does it change with age? (author's transl)].

We compared the excretory pancreatic function of a healthy young population (n = 18, mean age 31.8 years) with that of a healthy older people (n = 18, mean age 58.7 years) using a modified secretin-pancreozymin test which comprised short infusion of secretin, injection of pancreozymin, and repetition of this procedure immediately after the end of the collection period following the first stimulation. Secretion rate and bicarbonate following secretin, lipase, amylase and secretin rate following pancreozymin were significantly lower in the old than in the young after first and second stimulation. Trypsin was lower in the old than in the young following repeat stimulation. Trypsin was the only substance which was produced in smaller quantities after the second stimulation than after the first, i.e. pancreatic fatigue was demonstrable in the older age group.

Aging↗
PubMed1982

[Differential diagnosis of pancreatitis: metastasis to the pancreas].

A case report is given of a patient with a metastasizing teratocarcinoma of the testis (ripe teratoma and embryonal carcinoma), which was misinterpreted in the beginning as acute pancreatitis. At post mortem, metastases of this tumour were found in the pancreas, which apparently had led to inflammatory lesions of this organ, which could not explain however all of the clinical symptoms seen before. The literature dealing with cases suffering from acute pancreatitis induced by tumours is reviewed. A list of possible associations between pancreatitis and tumours is given.

Acute Disease↗
PubMed1981

[Can cerulein replace pancreozymin in the diagnosis of exocrine pancreatic function? (author's transl)].

The effect of the decapeptide cerulein on exocrine pancreatic function was compared with pancreozymin by means of intraindividual double stimulation. 100 ng/kg bw/45 min of synthetic cerulein led to a greater enzyme excretion than 2 U/kg bw pancreozymin. This increase in enzyme secretion was independent of whether the pancreas function was normal or disordered. In the selected experimental procedure, cerulein increased the excretion of enzymes (chymotrypsin, trypsin, lipase, amylase) whether it was infused in connection with or before an injection of pancreozymin. Cerulein can therefore completely replace pancreozymin in the diagnosis of pancreatic function.

Ceruletide↗
PubMed1981

[Patients with fatty liver. Study of ten years course of the disease (author's transl)].

Patients with fatty liver of grades I and II were re-examined by liver biopsy after a 10 years' interval. Only two patients showed improvement in the original findings. In each case up to about half of the material for investigation showed an unchanged stage of fatty liver or a deterioration. In the group with an unchanged clinical picture of grade II fatty infiltration and in the cases with a tendency to deteriorate, an accumulation of etiological factors was noted. Extensive histories proved that the patients had not altered their living habits in the past 10 years. This means that the prognosis of fatty liver with regard to regression of an originally established stage is very unfavorable, because the patients' understanding seems not to be very great.

Biopsy↗
PubMedDate not supplied

Effects of glucocorticoids on the regulation of the hypothalamic-pituitary-somatotropic system in depression.

In order to evaluate the possible effect of glucocorticoids as neuromodulators of the hypothalamic-pituitary-somatotropic system in depression, cortisol, growth hormone (GH), and insulin-like growth factor I (IGF-I) concentrations were studied before and after oral administration of 1 mg dexamethasone at 11 p.m. in 16 patients during depression and after recovery and in 28 healthy controls. While there were no significant differences in GH and IGF-I levels between depressed, recovered and control subjects, GH and IGF-I concentrations of cortisol non-suppressors were significantly elevated compared to suppressors. Moreover, post-dexamethasone cortisol, GH, and IGF-I levels were positively correlated. Dexamethasone had a stimulating effect on GH and IGF-I values in patients during depression and in cortisol non-suppressors only; this effect was absent in recovered and in control subjects and in cortisol suppressors. Thus, hypercortisolemia may be of great importance for the dysregulation of the hypothalamic-pituitary-somatotropic system reported in depression.

Adult↗
PubMedDate not supplied

Apoptosis and cell proliferation in the metaplasia-dysplasia-carcinoma-sequence of Barrett's esophagus.

BACKGROUND/AIMS: The regulation of apoptosis as a distinctive form of cell death and proliferation in the process of carcinogenesis in Barrett's esophagus is poorly understood. To investigate regulation of apoptosis, proliferation and the participation of the tumor suppressor gene p53, we examined these parameters in Barrett's metaplasia, dysplasia, and adenocarcinoma. METHODOLOGY: Apoptotic cells were identified and quantified in tissue specimens of 45 patients with different stages of Barrett's esophagus and normal fundus epithelium, respectively, using the in situ end-labeling and electron microscopy method in combination with morphological criteria. The tumor suppressor gene p53 was examined by direct sequencing of exon 4-8 as well as immunohistochemically. The proliferative activity was assessed by Ki67 immunostaining. RESULTS: Apoptotic cell death, identified by the in situ end-labeling and ultrastructural technique was significantly increased in Barrett's epithelium with intestinal metaplasia than in specimens with normal fundic epithelium and Barrett's carcinomas (P < 0.01). The proliferative activity, defined as Ki67 labeling index, was highest in adenocarcinomas (P < 0.01). P53 mutations were found in 8/9 adenocarcinomas and 2/5 specimens with dysplasia. Apoptosis was lower in p53 positive specimens of the metaplasia-dysplasia-carcinoma-sequence than in p53 negative specimens of Barrett's esophagus (P < 0.05). CONCLUSIONS: The higher levels of both apoptosis and proliferation indicate an increased cell turnover in Barrett's epithelium. Apoptosis seems to maintain tissue homeostasis, which is regulated by p53, and gradually lost in the metaplasia-dysplasia-carcinoma-sequence of Barrett's esophagus.

Adenocarcinoma↗