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Biomedical subjects

F Hajnal

Publications and source records attributed to F Hajnal.

30 records · Page 2Linked to original sources
PubMed1989

Mechanisms of action of alcohol administration on the trophic effect of soybean trypsin inhibitor and cholecystokinin octapeptide in rat.

Influence of alcohol administration on the trophic effect of cholecystokinin-octapeptide and soybean trypsin inhibitor administration was examined in male Wistar rats. Two x 4 mL of 20% alcohol given intragastrically during 2 wk did not significantly influence pancreatic weight, DNA, protein, trypsin, chymotrypsin, amylase, lipase, or trypsin inhibitor contents of the pancreas. It diminished the hypertrophy but not the hyperplasia seen after CCK-8 treatment, and eliminated the hyperplasia, as well as the hypertrophy provoked by SBTI administration. Secretory studies and CCK measurements demonstrated decreased CCK release in response to SBTI stimulation after 3-d alcohol administration. The results indicate that alcohol inhibits the enzyme synthesis of the CCK stimulated dividing and/or newly formed acinar cells and the endogenous CCK release.

Amylases↗
PubMed1989

Effect of alcohol and alcoholic beverages on nonstimulated pancreatic secretion in humans.

The effects of alcoholic beverages on pancreatic secretion, blood trypsin levels, the release of gastrin and cholecystokinin were studied and compared with those of an alcohol and a glucose solution. Studies were done on six healthy male volunteers. The trypsin level was measured in the duodenal aspirate, while blood trypsin and gastrin levels were measured by radioimmunoassay and the cholecystokinin level was measured by bioassay. Studies were done on 5 different days, and on each day, the effects of either a glucose solution; an alcohol solution; or wine, beer, and gin solutions infused into the stomach were compared. The glucose solution stimulated trypsin secretion (a threefold increase above the basal measure) and the release of cholecystokinin without changes in the blood trypsin level. Blood alcohol levels, after the alcohol solution and all alcoholic beverages, were similar, and subjects showed mild symptoms of intoxication. Pancreatic enzyme secretion and trypsin blood levels were not significantly affected by either alcohol or the alcoholic beverages. Wine and beer caused significant release of gastrin and cholecystokinin. Under the conditions of this study, which reproduce those of excessive alcohol drinking, alcohol and alcoholic beverages did not stimulate pancreatic enzyme secretion, although wine and beer increased the release of gastrin and cholecystokinin. We conclude that alcohol and alcoholic beverages do not affect nonstimulated pancreatic enzyme secretion.

Adult↗
PubMed1988

Pectin delays gastric emptying and increases satiety in obese subjects.

As pectin delays gastric emptying in normal subjects and satiety may be linked to the rate of gastric emptying, we designed this study to evaluate, in a group of obese subjects, the effect of adding pectin to a meal on gastric emptying, sensation of satiety, and postprandial plasma cholecystokinin and pancreatic polypeptide levels. We studied gastric emptying of solids in 9 adult obese subjects on 2 separate days in a randomized fashion. On day 1, 15 g of pectin was added to the meal, and on day 2 15 g of methylcellulose was added and served as control. Satiety was evaluated by an analogue rating scale. Pectin significantly delayed gastric emptying time [t1/2 = 116 +/- 23 min vs. 71 +/- 17 min observed with methylcellulose (p less than 0.001)]. Pectin also significantly increased subjects' sensation of satiety [98 +/- 7 vs. 74 +/- 17 (p less than 0.001)]. Postprandial release of cholecystokinin and pancreatic polypeptide was not modified by pectin. As pectin induces satiety and delays gastric emptying in obese patients, it may be a useful adjuvant in the treatment of disorders of overeating.

Adult↗
PubMed1984

Synthesis of potent heptapeptide analogues of cholecystokinin.

Nine new analogues of acetyl-CCK-heptapeptide (Ac-Tyr(SO3H)2-Met3-Gly4-Trp5-Met6-Asp7-Phe8-NH2 ) were synthesized by solid-phase methodology. In a first series, the Asp7 residue was replaced by hydroxy amino acid sulfate esters. In another series, Gly4 was substituted by D-Ala, while Trp5 and Met6 were replaced by their D enantiomer. The introduction of the sulfate ester was performed with a new, mild, crystalline, and stable reagent, pyridinium acetyl sulfate. Each analogue that contained Tyr(SO3H)2 and a hydroxy amino acid sulfate ester [Ser(SO3H), Thr(SO3H), or Hyp(SO3H)] in position 7 proved to be more potent (1.9, 1.7, and 3.0 times, respectively) than CCK-8 in vitro (isolated gallbladder strips). While devoid of gastrin-like activity in vivo, these analogues had potent anticonvulsive activity. The analogues containing a D-amino acid residue were less potent than the parent compound in vitro. The D-Ala4 replacement, however, yielded a compound that was 40% as potent as CCK-8 in the in vitro test but showed prolonged duration of action on sphincter Oddi. While the 7-substituted Ac-CCK heptapeptides are among the most potent CCK analogues reported so far, the D-Ala4 replacement resulted, for the first time, in prolonged activity in vivo.

Amino Acid Sequence↗
PubMed1983

Subcellular localization of bioactive cholecystokinin-like peptides in the rat cerebral cortex.

The subcellular distribution of cholecystokinin (CCK), especially its exact localization within the synaptosome, was studied in the rat cerebral cortex. Highest CCK-like bioactivity was measured in the synaptic membrane fractions, paralleling the distribution of (Na+ + K+)-dependent ATPase. In the synaptic vesicles, which were characterized by high acetylcholine content and by the absence of (Na+ + K+)-ATPase, only minimal quantities of CCK were detected.

Animals↗
PubMed1983

The diagnosis of hypertonic Oddi's sphincter dyskinesia.

The diagnostic possibility of hypertonic Oddi's sphincter dysfunction was evaluated in 100 cholecystectomized and 28 noncholecystectomized patients. An organic lesion interfering with free bile flow was ruled out in every case. The existence of the syndrome, i.e., the dysfunction of the Oddi's musculature, was verified using the morphine-choleretic test combined with either dynamic hepatobiliary scintigraphy or (in selected cases) percutaneous transhepatic cholangiography. Hypertonic Oddi's sphincter dyskinesia can be regarded as an independent clinical syndrome.

Ampulla of Vater↗
PubMed1981

Cholecystokinin-like bioactivity in rat cerebral cortex.

Cholecystokinin (CCK)-like bioactivity was studied in extracts of rat cerebral cortex by three different bioassays. Positive results were obtained by all procedures used. A fairly good quantitative correlation was found when testing the same extracts by two of the methods. A considerable amount of CCK-like activity was demonstrated in the various subcellular fractions (synaptic membranes, synaptic vesicles, and synaptic fragments) corresponding to synaptic structures. The results are in accordance with the findings of several authors who demonstrated CCK-like immunoreactivity in the brain, especially in the cortex. The use of three different bioassays in three species (rabbit, rat, dog) seems to prove that some bioactive molecular form of CCK exists in the brain, mainly in the cortical area. The findings that subcellular elements of the synaptic structures contain relatively high concentrations of CCK raises the question of the possible role of CCK in the neuronal transmission.

Animals↗
PubMed1979

Investigation of cholecystokinin-octapeptide splitting enzyme in dog kidney.

In vitro experiments were carried out to examine the enzymatic activity in various organ homogenates of the dog, which inactivates the biological activity of the synthetic cholecystokinin-octapeptide (CCK-OP). The highest splitting activity was found in the renal cortex; substantially lower activities were registered in the lung, pancreas and small intestine. It seems interesting that neither the gallbladder nor the saliva and the serum contained measurable amount of the CCK-OP splitting activity. An effort was made to characterize the CCK-OP inactivating principle found in the renal cortex. It was ascertained that the CCK-OP was inactivated by a peptidase which is heat sensitive, has a pH optimum of 7,4 and could be inhibited by chelating agents (EDTA) and epsilon-aminocaproic acid. The fact that most of the enzyme function is associated with the sediment obtained at 12 000 g speaks in favour of its mitochondrial origin.

Animals↗