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Biomedical subjects

B Simon

Publications and source records attributed to B Simon.

At least 361 records · Page 20Linked to original sources
PubMed1980

[Preadipocytes: a new model in obesity research (author's transl)].

The present knowledge about the differentiation of preadipocytes into adipocytes is reviewed. The adipose conversion is initiated by an as yet unknown serum factor and is enhanced by various hormones including insulin, prostaglandin F2 alpha, steroids, and prolactin; prostaglandin E1 and phorbol diesters are inhibitors of differentiation. Adipose conversion of fibroblasts (preadipocytes) is associated with the coordinate induction of key enzymes of the lipogenetic and lipolytic pathways and is accompanied by profound changes in hormone responsiveness. Pathophysiological studies with preadipocytes of genetically obese mice show differences between adipocyte precursors of obese animals and lean controls which may be casually related to obesity. Regional differences in the hormonal regulation of fibroblast conversion might be important for the sex differences of fat deposition in human beings.

Adipose Tissue↗
PubMed1980

[Active HCO3(-)Secretion in the gastric-mucosa. A causal factor in peptic ulcer disease? (author's transl)].

Studies during the last few years have revealed evidence of active secretion of HCO3(-) in the gastric mucosa both in vitro and in vivo. This transport process presumably has considerable importance for the protection of the gastric epithelium, disturbance must be considered a causal factor in the pathogenesis of gastric ulcer. The HCO3(-)-transport is subject to autonomic control. It is inhibited by drugs with an ulcerogenic action and stimulated by anti-ulcerogenic prostaglandins. The results available up to now raise the probability of the physiologic and pathophysiologic significance of the HCO3(-)-transport system. Clinical investigations must demonstrate the therapeutic efficacy of control of the alkali secretion in the gastric mucous membrane.

Biological Transport↗
PubMed1980

Inhibition of the stimulatory effect of adrenaline and prostaglandin E1 on the human fat cell adenylate cyclase by adenosine.

Adenosine is known to modulate adenylate cyclase activity in a variety of tissues. We have tested the effects of adenosine on basal activity and the catecholamine- or prostaglandin E1-stimulated activity of the human fat cell adenylate cyclase. Adenosine caused a dose-dependent inhibition of basal enzyme activity as well as of adrenaline-and prostaglandin E1-stimulated rates of 3',5'-cyclic AMP accumulation. The adenosine-induced inhibition was specific since other nucleosides or their respective nitrogenous parent bases, with the exception of adenine, failed to mimic the action of adenosine. In addition, the adenosine-induced inhibition could be reversed by inclusion of adenosine deaminase. The results are compatible with the concept of adenosine acting as an inhibitor of lipolysis at the level of the membrane-bound adenylate cyclase. They show that this nucleoside can also inhibit the prostaglandin E1-induced stimulation of the human fat cell adenylate cyclase thereby suggesting that the effects of adenosine and prostaglandins might be antagonistic under conditions where prostaglandins act as stimulators of lipolysis.

Adenosine↗
PubMed1980

Effects of salbutamol and butoxamine on the human fat cell adenylate cyclase.

In order to characterize the beta-adrenoceptors coupled to the human fat cell adenylate cyclase more extensively the effects of the beta 2-selective agonist salbutamol on basal and isoproterenol-stimulated rates of cAMP-accumulation were studied. Although exhibiting only low intrinsic activity salbutamol displayed only slightly lower affinity towards the beta-adrenoceptors linked to the human fat cell adenylate cyclase than isoproterenol. In addition, the beta 2-selective antagonist butoxamine was slightly more potent in inhibiting the isoproterenol-stimulated fat cell enzyme than the cardioselective beta-blocking agent practolol. These results further emphasize the difficulties in classifying the lipolytic response of adipose tissue to beta-adrenergic agonists and antagonists within a uniform beta-receptor theory.

Adenylyl Cyclases↗
PubMed1980

Interaction of laxatives with enzymes of cyclic AMP metabolism from human colonic mucosa.

The mechanism by which laxatives such as dioctyl sodium sulfosuccinate and ricinoleic acid evoke colonic fluid secretion has been suggested to involve mucosal cyclic AMP. Ricinoleic acid and dioctyl sodium sulfosuccinate were tested for their capacity to modulate the key enzymes of cAMP-metabolism--adenylate cyclase and cAMP-phosphodiesterase--in human colonic mucosa. Both laxatives were ineffective stimuli of human colonic adenylate cyclase. In contrast to ricinoleic acid, dioctyl sodium sulfosuccinate was a competitive inhibitor of soluble cAMP-phosphodiesterase activity. These experiments suggest that the cathartic properties of dioctyl sodium sulfosuccinate in human colonic mucosa might be mediated by cyclic AMP via inhibition of soluble phosphodiesterase activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Inhibition of human fat cell adenylate cyclase mediated via alpha-adrenoceptors.

Human adipose tissue contains alpha- as well as beta-adrenoceptor sites mediating antagonistic catecholamine effects on lipolysis. To characterize the mechanisms of catecholamine action in biochemical terms we have studied the effects of the almost pure beta-adrenoceptor agonist isoproterenol and of the mixed adrenergic agonist adrenaline on human fat cell adenylate cyclase in the presence of alpha- and beta-adrenoceptor blocking drugs. In contrast to the almost pure beta-adrenergic agent isoproterenol, the mixed agonist adrenaline, besides its stimulatory action, also had inhibitory effects which became apparent upon complete beta-adrenoceptor blockade using 0.05 mmol/l propranolol. Under these conditions adrenaline caused a dose-dependent inhibition of basal and parathyroid hormone-activated enzymic activity with a maximum of 30-50%, which was dependent on GTP and could be reversed by simultaneous alpha-adrenergic blockade using 5 mumol/l dihydroergotamine or 10 mumol/l phentolamine. These results support the concept of antogonistic alpha- and beta-adrenoceptor sites coexisting as regulatory subunits of the human fat cell adenylate cyclase.

Adenylyl Cyclase Inhibitors↗
PubMed1980

Human gastric mucosal adenylate cyclase activity: effects of various cytoprotective prostaglandins.

Several prostaglandins prevent ulcer formation (called cytoprotection) by a mechanism other than inhibition of gastric acid secretion. One suggestion is that they increase cyclic AMP in non-parietal cells. A variety of prostaglandins with potent cytoprotective properties were tested for their capacity to modulate adenylate cyclase activity in homogenates of human gastric mucosa. Prostaglandin E2, prostacyclin (PGI2) and 15(S)-methyl-PGE2 stimulated the cyclase in human gastric mucosal biopsy specimens in a dose-dependent manner. Cytoprotective prostaglandins without antisecretory properties such as PGF2 beta were also able to activate the enzyme system dose-dependently. In contrast, cytoprotective prostaglandins such as PGD2, the PGE1-analogue, SC-29333, and the prostaglandin-like compound C83 did not stimulate human gastric adenylate cyclase. Whereas PGD2 did not modulate enzyme activity at all, SC-29333 and C83, at concentrations greater than 10 mumol/l, inhibited basal and PGE2-stimulated enzyme activities. These studies suggest that cyclic AMP is not directly related to the cytoprotective effect of prostaglandins, at least in human gastric mucosa.

Adenylyl Cyclases↗
PubMed1980

Human colonic adenylate cyclase. Stimulation of enzyme activity by vasoactive intestinal peptide and various prostaglandins via distinct receptor sites.

The effects of meclofenamic acid on basal and hormone-stimulated adenylate cyclase in human colonic mucosa were tested. It is shown that meclofenamic acid is a relatively specific inhibitor of the stimulatory action of prostaglandins on the level of mucosal adenylate cyclase. This compound did not inhibit significantly the effects of vasoactive intestinal peptide (VIP) on the human enzyme system. VIP18-28 did not act as a partial agonist and did not inhibit the response to the intact VIP. Our studies suggest the existence of distinct receptor sites for both secretagogues (VIP and prostaglandins) in human colonic mucosa.

Adenylyl Cyclases↗
PubMed1980

PGI2-sensitive human adenylate cyclase in biopsy specimens of corpus, antral and duodenal mucosa.

The distribution of prostacyclin-(PGI2-)sensitive cyclase in human gastric and duodenal mucosa was studied. Like PGE2, PGI2 induced a dose-dependent increase of enzyme activity throughout the stomach and the duodenum. Maximal effects (about 2.5- to 3.0-fold increase) were observed at a PGI2 concentration of 0.28 mmol/l. The stable breakdown product 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) was much less active. The equal distribution of the PGI2-sensitive adenylate cyclase in the human upper alimentary tract suggests a localization of this enzyme system in cells not directly related to gastric acid secretion.

Adenylyl Cyclases↗
PubMed1980

[Influence of ranitidine on antipyrine metabolism (author's transl)].

Antipyrine kinetics were determined in 6 healthy volunteers before and after the end of a 1 week treatment period of ranitidine 150 mg twice a day. The mean antipyrine half-life (h) was before 12.6 +/- 4.6 h and after ranitidine treatment 12.0 +/- 2.6 h. Antipyrine clearance (ml/min) and volume of distribution (1) were not altered following ranitidine administration. The results suggest that ranitidine has no influence on antipyrine-metabolism in healthy volunteers.

Adult↗