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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1979

Effects of some naturally occurring prostaglandins of the D-, E-, and I-type and synthetic analogues on adenylate cyclase of human fat cell ghosts.

The effects of various prostaglandins originating from arachidonic acid (prostaglandin E2, D2, I2) as well as of methylated analogues of prostaglandin E2 (16,16-dimethyl prostaglandin E2 and 15-S-methyl prostaglandin E2) on the human fat cell adenylate cyclase were studied. In addition, the stable breakdown product of prostaglandin I2, prostaglandin 6-keto-F1-alpha, was tested for activity. Prostaglandin E2 and its methylated analogues as well as prostaglandin D2 and I2 were active stimulators of the human fat cell enzyme. The stable breakdown product of prostaglandin I2 (prostaglandin 6-keto-F1-alpha) which is biologically inactive had no stimulatory effects, suggesting that stimulation of the human fat cell function. The stimulatory action of prostaglandin D2 is consistent with the elevation of cAMP-levels induced by this compound in intact fat cells. It is concluded that the stimulatory effects of prostaglandins on the human fat cell adenylate cyclase are related to their stimulatory effects upon lipolysis.

Adenylyl Cyclases↗
PubMed1979

Prostaglandin-sensitive adenylate cyclase in human gastric mucosa. Inhibition by nonsteroid anti-inflammatory agents.

The effects of various nonsteroid anti-inflammatory compounds on human gastric mucosal adenylate cyclase were tested. It is shown that fenamates, indomethacin and diclofenac-Na were relatively specific inhibitors of prostaglandin E2 action at the level of the mucosal cyclase activity. The results suggest that inhibition of prostaglandin E2-activated adenylate cyclase might at least in part contribute to the ulcerogenic effects of certain nonsteroid anti-inflammatory drugs.

Adenylyl Cyclases↗
PubMed1979

Modulation of human gastric mucosal adenylate cyclase activity by prostacyclin.

Prostacyclin, its stable metabolite 6-keto-prostaglandin F1 alpha and prostaglandin E2 were tested on the adenylate cyclase system in human gastric mucosa. All three compounds were able to activate human cyclase. Saturating concentrations of prostacyclin, prostaglandin E2 and 6-keto-prostaglandin F1 alpha (each 0.28 mM) increased the enzyme activity 3.0 and 1.6 fold, respectively. The concentrations of prostacyclin and prostaglandin E2 required to produce half maximal activation were in the same range. Prostacyclin is an efficient stimulator of human gastric mucosal adenylate cyclase.

Adenylyl Cyclases↗
PubMed1979

Biphasic effects of prostaglandin E2 on the human fat cell adenylate cyclase.

Adenylate cyclase of human fat cell ghosts shows a biphasic response towards prostaglandin E2 with inhibition occurring at nanomolar concentrations of the hormone and stimulation at concentrations beyond 10(-6) mol/liter. The expression of the inhibitory effect is critically dependent on GTP. Under the conditions employed (1 mmol/liter ATP, 5 mmol/liter Mg2+, 30 degrees C) the inhibitory component of prostaglandin E2 became apparent at GTP concentrations exceeding 10(-6) mol/liter. The prostaglandin E2-induced inhibition displayed characteristic features of prostaglandin action in intact fat cells with respect to the effective concentrations and degree of inhibition. It is concluded that prostaglandin E2 is capable of inducing antagonistic effects upon lipolysis via interaction with the membrane-bound adenylate cyclase.

Adenylyl Cyclases↗
PubMed1979

Antagonistic effects of prostaglandin E1 and nicotinic acid on the human fat cell adenylate cyclase.

Both prostaglandin E1 and nicotinic acid markedly reduce 3',5'-cyclic AMP-accumulation and lipolysis in adipose tissue. These effects were assumed to be mediated via inhibition of the fat cell adenylate cyclase. Therefore, the effects of prostaglandin E1 and nicotinic acid on the human fat cell adenylate cyclase were compared. Prostaglandin E1 caused a dose-dependent stimulation of the enzyme, whereas nicotinic acid was found to act as an unspecific inhibitor depressing all expressions of enzyme activity including prostaglandin E1-stimulated rates of 3',5'-cyclic AMP formation. It is concluded that the common metabolic effects of nicotinic acid and prostaglandin E1 are unlikely to be mediated via the membrane-bound adenylate cyclase in human adipose tissue.

Adenylyl Cyclase Inhibitors↗
PubMed1978

[Obesity and adipose tissue. 2. Hormonal regulation of adipose tissue metabolism].

The effects of hormones on human adipose tissue are reviewed with respect to the pathogenesis, prevention and therapy of obesity. Insulin. The insulin-resistance in the obese is associated with a decrease of the number of insulin receptor sites, which is likely to be secondary to increased insulin levels. Catecholamines. Human adipose tissue contains alpha- and beta-adrenergic receptors. Alterations in the relation of alpha- and beta-adrenergic responsiveness may be important in the pathogenesis of regional forms of obesity. Gastrointestinal hormones. As opposed to adipose tissue of other species lipolytic effects of gastrointestinal hormones were as yet not clearly demonstrated in human fat cells. Prostaglandins were implicated in the pathogenesis of metabolic obesity. However, the effects of these C-20 fatty acids on human adipose tissue remain to be elucidated. Parathyroid hormone has been shown to possess lipolytic activity in vitro. This property may be important under physiological conditions too. Triglyceride storage diseases and lipomatoses are discussed as models for studying impaired hormonal responsiveness in human adipose tissue.

Adipose Tissue↗