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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 91 records · Page 5Linked to original sources
PubMed1981

Adenylate cyclase of multiple lipomata. Regional differences in adrenaline-responsiveness.

Multiple symmetric lipomatosis has been proposed to be associated with impaired catecholamine-responsiveness of hypertrophic adipose tissue at the level of beta-adrenergic receptors or adenylate cyclase respectively. We have studied the regulation of the adenylate cyclase by guanine nucleotides and adrenaline in 5 subjects suffering from multiple encapsulated lipomata. In the presence of GTP (0.1 mmol/l) basal adenylate cyclase activity averaged 0.5 +/- 0.3 nmol cAMP/mg protein/10 minutes in normal adipose tissue and 1.0 +/- 0.4 nmol cAMP/mg protein/10 minutes in hypertrophic adipose tissue respectively. The synthetic GTP-analogue GMP(PNP) (0.1 mmol/l) increased non-stimulated activity by about 100% in both tissues. Adrenaline (1 mumol/l-1 mmol/l) caused a dose-dependent increase of enzymic activity in both tissues which had a maximum of 130% above basal levels in the presence of GTP and of 300% in the presence of GMP(PNP) respectively. In one of the six subjects suffering from gluteal lipomata normal adipose tissue was obtained from the gluteal as well as the abdominal region on two occasions. Maximally effective concentrations of adrenaline (1 mmol/l) induced a 3-fold increase of enzymic activity in abdominal membranes compared with about a 1.7- and 1.75-fold increase in normal and lipomatous tissue from the gluteal region. The results show that encapsulated lipomata contain a normally reactive adenylate cyclase system.

Adenylyl Cyclases↗
PubMed1981

Effects of prostaglandin E2 on adenylate cyclase activity and lipolysis in human adipose tissue.

To elucidate the mechanisms of prostaglandin action in human adipose tissue the effects of prostaglandin E2 on isoproterenol-stimulated lipolysis in intact human fat cells and on adenylate cyclase activity of fat-cell ghosts were compared. In intact fat cells prostaglandin E2 caused a dose-dependent inhibition of isoproterenol -stimulated lipolysis which has a maximum of about 40 per cent; half maximal effects were observed at approximately 30 nmol/l prostaglandin E2. In broken cell preparation prostaglandin E2 displayed biphasic effects on adenylate cyclase activity with inhibition occurring in the nanomolar concentration range and stimulation at prostaglandin E2-concentrations above 1 mumol/l. The inhibitory component of prostaglandin E2-action was critically dependent on relatively high concentrations of GTP (greater than 1 mumol/l) and was augmented by sodium ions. The inhibitory component of prostaglandin E2-action on adenylate cyclase reflected the antilipolytic effects of this C-20 fatty acid in intact fat cells with respect to the effective concentration range and degree of inhibition suggesting that the antilipolytic effects of prostaglandins are in fact mediated via inhibition of human fat-cell adenylate cyclase.

Adenylyl Cyclases↗
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↗