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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 19 recordsLinked to original sources
PubMed1992

Human fat cells possess a plasma membrane-bound H2O2-generating system that is activated by insulin via a mechanism bypassing the receptor kinase.

Insulin caused a transient increase in H2O2 accumulation in human fat cell suspensions that was observed only in the presence of an inhibitor of catalase and heme-containing peroxidases, such as azide, and reached peak levels of 30 microM within 5 min. The cells contained a plasma membrane-bound NADPH oxidase, producing 1 mol H2O2/mol of NADPH oxidation, that was activated on exposure of intact cells to insulin at contrations that are physiologically relevant (0.1-10 nM). The hormone effect was rapid and was due to a selective increase in substrate affinity. The enzyme was magnesium dependent, required a flavine nucleotide for optimal activity, and was most active at pH 5.0-6.5. In contrast to all other hormone- or cytokine-sensitive NADPH oxidases that have been characterized in sufficient detail, the human fat cell oxidase retained its hormone responsiveness after cell disruption, and only Mn2+, but no ATP, was required for a ligand-induced activation in crude plasma membranes. The results demonstrate that insulin utilizes tyrosine kinase-independent pathways for receptor signaling and strongly support the view that H2O2 contributes to the intracellular propagation of the insulin signal.

Adenosine Triphosphate↗
PubMed1990

Beta-adrenergic stimulation of adenine nucleotide catabolism and purine release in human adipocytes.

The effects of beta-adrenergic agonists on ATP utilization and adenine nucleotide breakdown in human adipocytes were examined. The catecholamine-induced increase in cAMP was associated with an enhancement of adenine nucleotide catabolism resulting in an increase in release of inosine and hypoxanthine which can not be reutilized for adenine nucleotide synthesis. Therefore, one-third of total cellular adenine nucleotides were irreversibly lost in the presence of 1 mumol/liter isoproterenol. The catecholamine-induced increase in purine release could be blocked by phosphodiesterase inhibitors, suggesting that cAMP is the main precursor of purines in the presence of beta-adrenergic agonists. However, epinephrine (in the simultaneous presence of the alpha 2-adrenergic blocking agent, yohimbine) and isoproterenol were 10 times more potent in stimulating purine release than in elevating cAMP. In addition, purine release ceased when cAMP was still markedly increased, suggesting a compartmentation of the cyclic nucleotide and/or involvement of the hormone-sensitive, low Km cAMP phosphodiesterase. The results document that white fat cells have an enormous potential for dissipating energy, and demonstrate that the pathway involving cAMP formation and hydrolysis constitutes the principle route of adenine nucleotide catabolism in the presence of beta-adrenergic agonists.

1-Methyl-3-isobutylxanthine↗
PubMed1979

[Inhibition of pentagastrin-stimulated gastric secretion by ranitidine (author's transl)].

The dose-effect relationship of ranitidine, a recently developed selective histamine H2 receptor antagonist was tested on six healthy subjects after oral administration. Ranitidine gave dose-dependent inhibition of pentagastrin-stimulated acid secretion. Half-maximal inhibition occurred at 75 mg. The antisecretory effect was still demonstrable five hours after oral intake. The drug is thus more powerful and has more lasting antisecretory action, even after oral intake, than cimetidine.

Adult↗
PubMed1979

[Peptic ulcer disease and primary hyperparathyroidism (author's transl)].

The causal relationship of primary hyperparathyroidism and ulcer disease is reviewed. In contrast to earlier ideas careful clinical and clinico-chemical investigations have shown that in patients with manifest primary hyperparathyroidism neither is the incidence of ulcer disease raised nor are deviations from the normal behavior of acid secretion or the serum gastrin level to be observed in comparison with the average population.

Calcium↗
PubMed1979

[Treatment of cimetidine-resistant gastric ulcer with carbenoxolone-sodium (author's transl)].

Case report on a successful treatment of a cimetidine-resistant gastric ulcer with carbenoxolone-Na. Administration of 1.0g cimetidine/d over a period of 8 weeks failed to reduce gastric ulcer size. Subsequent therapy with carbenoxolon-Na caused a complete healing of the gastric ulcer within 4 weeks. This case is discussed with respect to the possible advantages of a combined regimen with drugs of different mechanisms of action.

Aged↗
PubMed1979

Activation of human large bowel adenylate cyclase by methylated prostaglandin E2 analogues.

The effects of methylated analogues of prostaglandin E2 upon the adenylate cyclase system in human colonic mucosa were tested. 16,16-dimethyl-prostaglandin E2 and 15-(S)-methyl-prostaglandin E2 increased the cyclase system in a dose-related manner. Maximal stimulation (about 250%) of enzyme activity occurred at a prostaglandin analogue concentration of 0.1 g/l. Diarrhea seen in patients treated with these orally effective prostaglandin analogues might in part be explained by activation of large bowel adenylate cyclase which is supposed to play a key role in the secretory process in this organ.

Adenylyl Cyclases↗