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Biomedical subjects

M Peterlik

Publications and source records attributed to M Peterlik.

At least 91 records · Page 5Linked to original sources
PubMed1983

Vitamin D stimulates (Na+ + K+)-ATPase activity in chick small intestine.

Vitamin D3 and 1,25-dihydroxyvitamin D3 raise (Na+ + K+)-ATPase activity (ouabain-sensitive 86Rb+ uptake) in cultured embryonic and 4-week-old chick small intestine. Vitamin D stimulation of the sodium pump, which requires genomic action of the sterol, may lead to enhanced Ca2+ extrusion via a basolateral Na+/Ca2+ exchange mechanism, and, in addition, may provide a proliferative signal in undifferentiated enterocytes.

Animals↗
PubMed1982

Differential response of enterocytes to vitamin D during embryonic development: induction of intestinal inorganic phosphate, D-glucose and calcium uptake.

Chick intestine maintained in organ culture at day 20 of embryonic life responds to appropriate dose levels of 1,25-dihydroxyvitamin D3 or vitamin D3 in the culture medium by stimulation of Na+-dependent uptake of inorganic phosphate (Pj) and D-glucose as well as by increased calcium absorption. The intensity of each single response to vitamin D varies along the small intestine: Only the jejunum shows high vitamin D increments of all three transport systems under investigation. Inhibition of vitamin D responses by actinomycin D suggests the involvement of gene activation in the sterol's action of raising intestinal transport activities. Determination of the developmental pattern of each vitamin D-dependent transport system showed that only calcium absorption could be induced in undifferentiated cells on day 15, while complete expression of vitamin D action, including elevation of Na+-dependent uptake of D-glucose and Pj, required a fairly advanced state of epithelial maturation and was thus not observed before the final day 20 of embryonic development. This indicates a progressive change of hormone sensitivity of absorptive cells during differentiation.

Animals↗
PubMed1979

Interference of tris(hydroxymethyl)aminomethane with structure and function of Golgi membranes.

Short term perfusion of isolated rat liver with tris(hydroxymethyl)aminomethane or other nonamphoteric amines (glycine amide, diethylamine) in moderate concentrations (10 to 20 micron) causes blistering of Golgi stacks on the concave side as well as swelling of lysosomes and of secretory vesicles in otherwise unaltered hepatocytes. Similar vacuolization is observed in Kupffer cells, pancreatic beta-cells, intestinal epithelial cells, and renal proximal tubule cells, but not in alpha-cells of the pancreas or in kidney glomerular podocytes. Fusion of the vesicles occurs frequently and involves denudation of intramembranous particles from contact areas. Since protein synthesis is not affected, inhibition by tris(hydroxymethyl)aminomethane of protein secretion into the perfusate indicates a block in protein processing at a postribosomal level. This finding together with morphologic evidence unravels the Golgi and post-Golgi membranes as specific site of tris(hydroxymethyl)aminomethane interaction with intracellular structures.

Animals↗
PubMed1978

Phosphate transport by embryonic chick duodenum. Stimulation by vitamin D3.

Embryonic chick duodenum maintained in organ culture is a well-suited model for the study of vitamin D effects on inorganic phosphate (Pi) absorption. The system is sensitive to as little as 6.5 nM vitamin D3 (0.1.I.U./ml culture medium). Increased phosphate absorption is observed after 6--12 h of culture. Maximal response (133% of vitamin D-efficient control) is achieved at 24 h. Phosphate uptake by embryonic chick duodenum involves a saturable and a non-saturable component. The former displays characteristics of an active sodium-dependent transport mechanism and is also sensitive to vitamin D3. Presence of the sterol in culture medium raises the maximal velocity from 55 to 75 nmol Pi/min per g tissue. Km remains unchanged (0.5 mM Pi). Duodena cultured in presence of inhibitors of protein synthesis (actinomycin D, alpha-amanitin and cycloheximide) display reduced rates of phosphate absorption. This treatment also prevents vitamin D3 action on phosphate transport. It is concluded that the sterol affects phosphate transport by modulation of synthesis of proteins which are functional in the Pi absorptive process.

Animals↗
PubMed1978

Stimulatory effect of 1,25-dihydroxycholecalciferol-like substances from Solanum malacoxylon and Cestrum diurnum on phosphate transport in chick jejunum.

Extracts of the calcinogenic plants Solanum malocoxylon and Cestrum diurnum stimulate phosphate absorption by the jejunum of vitamin D-deficient chicks, as determined by everted gut sac technique. Their action on cellular pathways of transepithelial phosphate transport is indistinguishable thereby from that of cholecalciferol. Increased net absorption from the lumen was due to enhanced uptake of phosphate from the luminal side, while leakage of tissue phosphate in the opposite direction was apparently unaffected. Steep serosa/mucosa concentration gradients were observed as consequence of enhanced levels of transepithelial phosphate flux in the mucosa-to-serosa direction. With respect to their stimulatory action on phosphate absorption, the calcinogenic plant factors retained their biological activity when phosphate transport was depressed by a high strontium diet. Their action in overcoming the strontium inhibition of phosphate absorption, calcium-binding protein synthesis, and alkaline phosphatase activity, was comparable to the effect of 1,25-dihydroxycholecalciferol. On the basis of these biological responses, the action of the plant factors from Solanum malacoxylon and Cestrum diurnum provides further evidence for their close resemblance to the hormonally active sterol.

Animals↗
PubMed1977

[Experimental cholestasis by dibucaine and harmaline: effects on bile flow and hepatic transport of bile acids, ethacrynic acid and ouabain (author's transl)].

For further confirmation of the hypothesis that bile-salts independent bile flow depends on transepithelial Na+ fluxes, the effect of dibucaine (0.5 to 1.6 mM) and of harmaline (1.7 to 4.0 mM) on bile formation was studied in the isolated rat liver. Both compounds, which are known to inhibit passive Na+ entry into tissues other than liver, inhibit bile secretion in a dose-dependent fashion. Measurements of oxygen consumption and examination of liver tissue by electronmicroscopy exclude unspecific damage to liver cells as the cause for secretory failure. Cholestasis induced by dibucaine and harmaline is reversible upon wash-out of the drugs from the perfusion system. Simultaneously added choleretics, such as taurocholate, cholate, ethacrynic acid or ouabain, fail to elicit a secretory response. Since harmaline is an inhibitor of Na+-dependent transport processes, its effect and that of dibucaine on Na+-linked uptake of these choleretics by the isolated liver was determined. Harmaline and dibucaine reduce taurocholate transfer to the extent of the Na+-independent fraction only, but completely inhibit active entry of cholate, ethacrynic acid and ouabain. It is concluded that drug-membrane interactions primarily on the sinusoidal surface but possibly also at the canalicular pole of the hepatocytes are responsible for the impairment of basal and stimulated bile secretion.

Alkaloids↗