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PubMed1975

[Studies on the culture of clostridium butyricum strain M 55 ATCC 13.732. 4th Communication: The influence of peptone quality upon kininase activity (author's transl)].

Studies of the oncolytic effect of Cl. butyricum strain M 55 resulted in the hypothesis of oncolysis to be an effect of a continuous production of kinin-decomposing enzymes. A decomposition of bradykinin will reduce capillary permeability and microcirculation in the tumour tissue, thus releasing and maintaining the process of necrotization. To achieve an optimal oncolytic effect of Cl. butyricum M 55, in addition to conditions already demanded in preceding papers, also an abundant production of kininase is required. Experience has shown peptone-containing media to be most suitable for culturing the M 55 strain, kininase formation being dependent upon peptone quality. The best yield of kinine-decomposing enzymes was achieved with the following peptones: peptone from Gelatine Merck, Tryptose Merck, Microbiotone Oxoid, Proteose Oxoid and Trypticase BBL. To obtain the greatest possible kininase production by the spores of Cl. butyricum M 55 applied for oncolytic therapy, the peptones mentioned are recommended for culture.

Bradykinin↗
PubMedDate not supplied

[Preparation and testing of Sardinella peptones: application to lipase production by Staphylococcus sp].

Production of lipase by Staphylococcus sp. in media containing fish peptones from sardinelle (Sardinella aurita) prepared in the laboratory was studied. Lipase production is strongly affected by lipids present in fish flours. Fish peptones prepared from dIgresed whole flesh was an excellent substrate for lipase production. A comparison of lipase production in media containing fish peptones or high quality commercial peptones indicated that fish peptones enhanced enzyme formation.

Animals↗
PubMed1981

Gastric acid and gastrin response to decaffeinated coffee and a peptone meal.

We compared five graded doses of decaffeinated coffee and a widely used protein test meal (Bacto-peptone) as stimulants of acid secretion (intragastric titration) and gastrin release (radioimmunoassay) in eight healthy men. In each subject, for both acid and gastrin, the sums of the responses to all five doses were greater to decaffeinated coffee than to peptone. The mean +/- SE peak acid output in millimoles per hour was 18.5 +/- 2.9 to decaffeinated coffee and 14.7 +/- 2.7 to peptone, representing 70% and 55%, respectively, of the peak acid output to pentagastrin. The mean +/- SEM peak increment over basal rate in serum gastrin in picograms per milliliter was 84.8 +/- 4.4 to decaffeinated coffee and 44.8 +/- 2.1 to peptone. At equal concentrations, decaffeinated coffee was a more potent stimulant of acid secretion and of gastrin release than peptone. The ingredient(s) of decaffeinated coffee that accounts for its high potency in stimulating acid secretion and gastrin release has not been identified.

Adult↗
PubMed1982

Release of gastric inhibitory peptide following a peptone meal in the dog.

Release of gastric inhibitory peptide into the circulation after peptone ingestion has not been demonstrated previously. In the present studies, 5 alert dogs with indwelling polyethylene portal venous catheters and gastric fistulas were studied. A meal of 10% peptone in 150 ml 0.9% NaCl, pH 7 was infused through the gastric fistula into the stomach. Gastric inhibitory peptide was measured by a specific and sensitive radioimmunoassay in sera obtained simultaneously from portal and cephalic veins before and at 1, 4, 8, 15, 30, 60, and 90 min after peptone infusion. Cephalic venous serum insulin and glucose concentrations were measured at the same time points. Mean basal portal and cephalic vein serum gastric inhibitory peptide concentrations were 136 +/- 22 and 34 +/- 10 (SEM) pg/ml, respectively. After infusion of the peptone meal, immediate increases in serum gastric inhibitory peptide levels were noted in both portal and peripheral circulation, with a peak of 597 +/- 151 pg/ml (p less than 0.02) at 8 min in portal venous serum and 323 +/- 95 pg/ml (p less than 0.05) at 15 min in cephalic venous serum. No significant increases in peripheral venous serum insulin concentration were detected throughout the entire collection period, whereas peripheral venous serum glucose levels increased slightly from a fasting level of 56 +/- 5 mg/dl to 72 +/- 5 mg/dl (p less than 0.05) at 90 min. The mean half-time of disappearance of intravenously administered gastric inhibitory peptide was found to be 7.6 +/- 1.5 (SEM) min. Results of these studies demonstrate prompt stimulation of gastric inhibitory peptide response to peptone, with peak serum gastric inhibitory peptide concentrations which are higher and occur earlier in portal than in peripheral blood. Gastric inhibitory peptide was found to have a brief half-time of disappearance, similar to that of other structurally related gastrointestinal peptides.

Animals↗
PubMed1982

[Antacids: A comparison of their in vitro neutralizing capacity in hydrochloric acid and in acidified peptone solution (author's transl)].

Using a simple and reproducible in vitro-test the neutralizing capacity of different liquid commercial antacids was measured at pH 2.0 and at pH 3.5 in diluted hydrochloric acid and in acidified peptone solution. In peptone solutions corresponding to postprandial gastric juice, antacids containing aluminum hydroxide and aluminate forming components demonstrated a marked loss in their neutralizing capacity when compared to peptone free hydrochloric acid as control. This loss in buffering capacity is dependent on the reaction time, the pH of the reaction mixture, the concentration of peptone in the solution and the amount of aluminum in the different antacid compounds. Furthermore the neutralizing capacity of aluminum hydroxide is also diminished by dibasic organic acids which mimicked fasting gastric juice in the experiment. The different availability of neutralizing potency of aluminum hydroxide containing antacids in acid and in acidified peptone solution will need to be considered when antacids are recommended for the treatment of patients with peptic ulcer disease.

Aluminum Hydroxide↗
PubMed1977

[Comparative study of the physico-chemical properties of peptones used to the production of dry alkaline agar for cholera diagnosis].

The authors present the results of chemical and physico-chemical study of dry peptones (made in the USSR) used in the production of dry alkaline nutrient agar for the diagnosis of cholera, in comparison with peptones used for other purposes. The batches and types of peptones studied differed by the fractional peptide composition and by the physico-chemical characteristics. Positive results were obtained in the biological test in using peptones with marked hydrolysis with the amine nitrogen content of not less than 200--230 mg%, with an elution curve approaching the Hottinger's peptone curve, well soluble in buffer phosphate solution at 5% concentration.

Animals↗
PubMed1996

[Capsaicin-sensitive afferent neurons and endogenous nitric oxide (NO) mediate the gastric acid secretion and hyperemic responses to intragastric peptone].

Using hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and a high dose of capsaicin to ablate the capsaicin-sensitive afferent neurons, the role of capsaicin-sensitive neurons in the gastric acid secretion and hyperemic response to intragastric peptone was investigated. The results were as follows: (1) there was an increase in acid secretion associated with the hyperemic response to intragastric peptone; (2) pretreatment with a high dose of capsaicin to ablate afferent neurons completely abolished the gastric hyperemic response to intragastric peptone and partially inhibited the acid secretion; (3) the gastric hyperemic response to intragastric peptone was completely blocked by pretreatment with L-nitro-arginine methyl ester (L-NAME), whereas the acid secretion was significantly attenuated; (4) inhibited effects of L-NAME on acid secretion and GMBF could be reversed by pretreatment with L-arginine (L-ARG); (5) pretreatment with atropine inhibited gastric acid output (GAO) and partially attenuated GMBF. These results suggested that capsaicin-sensitive afferent neurons and endogenous NO were involved in the gastric acid secretion and hyperemic response to intragastric peptone and the hyperemic response was mediated by both cholinergic and noncholinergic neurons.

Animals↗
PubMed2004

Ram horn peptone as a source of citric acid production by Aspergillus niger, with a process.

The present study deals with the production of citric acid from a ram horn peptone (RHP) by Aspergillus niger NRRL 330. A medium from RHP and a control medium (CM) were compared for citric acid production using A. niger in a batch culture. For this purpose, first, RHP was produced. Ram horns were hydrolyzed by treatment with acids (6 N H(2)SO(4), 6 N HCl) and neutralizing solutions. The amounts of protein, nitrogen, ash, some minerals, total sugars, total lipids and amino acids of the RHP were determined. RHP was compared with peptones with a bacto-tryptone from casein and other peptones. The results from RHP were similar to those of standard peptones. The optimal concentration of RHP for the production of citric acid was found to be 4% (w/w). A medium prepared from 4% RHP was termed ram horn peptone medium (RHPM). In comparison with CM, the content of citric acid in RHPM broth (84 g/l) over 6 days was 35% higher than that in CM broth (62 g/l). These results show that citric acid can be produced efficiently by A. niger from ram horn.

Animals↗
PubMed1988

Effect of mifentidine on peptone meal-stimulated gastric acid secretion and plasma gastrin levels in duodenal ulcer patients.

Mifentidine is a new H2-receptor antagonist with distinct characteristics of potency and long plasma half-life. The aim of this study was to evaluate the effects of mifentidine on peptone meal-stimulated gastric acid secretion. Nine duodenal ulcer patients in remission were enrolled in the study and given in double-blind and at random, on two different occasions, a single tablet of 10 or 20 mg mifentidine or placebo according to an incomplete balanced block design. Ninety min after ingestion of the drug, basal gastric secretion was collected for 30 min and volume, pH and acid output determined. Thereafter, the acid output following peptone meal-stimulation was measured for 2 h by a modified version of the intragastric titration method of Thompson and Swierczek. Plasma samples were collected for gastrin and mifentidine determinations. Basal acid output was strongly inhibited by both the low dose (-78%) and the high dose (-98%) (p less than 0.01). The peptone meal-stimulated acid output was reduced in a dose-dependent manner (-45% by 10 mg and -90% by 20 mg). The drug did not affect the fasting serum gastrin levels but increased, although not significantly, the gastrin response to food. The log of the area under the mifentidine plasma levels correlated linearly with total acid output (p less than 0.01). The results of this study indicate that mifentidine dose-dependently suppresses basal acid secretion and reduces peptone-stimulated gastric acid secretion in duodenal ulcer patients.

Adult↗
PubMed1982

Portal and cephalic venous gastrin after peptone infusion in the alert dog.

A model was designed to permit sampling of portal venous blood in nonanesthetized dogs. Five mongrel dogs were prepared with indwelling portal venous catheters and gastric fistulas. After a minimum recovery period of 7 days, a 10 percent peptone meal was infused into the stomach. Portal and peripheral venous sera were obtained in the basal state and at various time points after intragastric peptone infusion. Serum gastrin concentrations were later measured by radioimmunoassay. Mean basal gastrin from portal and peripheral venous sera were 17 +/- 5 and 13 +/- 2 pg/ml, respectively. After peptone infusion, a biphasic gastrin response was observed. The first peak in portal venous serum occurred at 2 minutes, increasing to 49 +/- 20 pg/ml, while in the peripheral venous serum, the initial peak occurred at 4 minutes to 33 +/- 4 pg/ml. The second peak component occurred at 30 minutes in both circulations, increasing to 35 +/- 14 pg/ml in portal venous serum and to 29 +/- 8 pg/ml in peripheral venous serum. The results of this study (1) demonstrate that the release of gastrin after a peptone meal in the dog is prompt and biphasic, and (2) provide an effective method for obtaining simultaneous portal and peripheral venous blood for measurement of gastrointestinal peptides in alert, nonanesthesized dogs.

Animals↗
PubMed1993

Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric acid secretion in conscious rats.

With the availability of selective gastrin/CCKB (L365,260) and CCKA (L364,718) receptor antagonists the present study was designed to investigate the role of gastrin and cholecystokinin (CCK) receptors in meal-stimulated gastric acid secretion. Gastric acid output was measured by continuous intragastric titration in conscious rats. Vehicle (dimethylsulfoxide/saline, 3:1), L365,260 (3 or 9 mg/kg), or L364,718 (1 mg/kg) was given by i.v. bolus injection. Basal acid output was strongly inhibited by both doses of L365,260 while L364,718 had no effect. Intragastric peptone (4%, w/v) increased acid secretion 40-65% of the response to a maximal dose (2.5 nmol/kg per h) of gastrin-17. L365,260 completely abolished gastrin-17 stimulated acid secretion and partially inhibited peptone-induced acid secretion. Blockade of CCKA receptors by L364,718 did not affect peptone-stimulated acid output. This study demonstrates that gastrin/CCKB receptors are important in regulating basal acid secretion in the conscious rat while CCKA receptors do not appear to influence basal or peptone-stimulated gastric acid secretion. Blockade of gastrin/CCKB receptors partially inhibits intragastric meal-stimulated acid secretion indicating that the gastrin/CCKB receptor has a physiological role as mediator of food-stimulated acid secretory response in conscious rats.

Animals↗
PubMed2000

Selective action of a CCK-B/gastrin receptor antagonist, S-0509, on pentagastrin-, peptone meal- and beer-stimulated gastric acid secretion in dogs.

BACKGROUND: The pharmacological effects of a novel CCK-B/gastrin receptor antagonist, S-0509, on gastric acid secretion in dogs remain unknown. AIM: To evaluate the antisecretory effects of S-0509 on gastric acid secretion and to compare such effects with famotidine or atropine in dogs stimulated with various gastric stimulants. METHODS: Ten beagle dogs with a denervated Heidenhain pouch and three beagle dogs with an innervated gastric fistula were used. Gastric acid secretion was stimulated by either continuous intravenous administration of pentagastrin, carbachol or histamine, or oral administration of a peptone meal or beer. RESULTS: In the Heidenhain pouch model, both intravenously administered and orally administered S-0509 significantly inhibited the gastric acid secretion stimulated by pentagastrin, peptone meal and beer. Nonetheless, the drug had little or no effect on carbachol-stimulated or histamine-stimulated acid secretion. Famotidine extensively inhibited all gastric acid secretion stimulated by the above stimulants in a non-selective manner. Atropine also significantly inhibited the acid secretion stimulated by pentagastrin, peptone meal, beer or carbachol, but was not able to inhibit stimulation due to histamine. Oral administration of peptone meal or beer significantly increased the plasma gastrin level. Similarly to the Heidenhain pouch model, even in the gastric fistula (GF) model, S-0509 significantly inhibited pentagastrin-stimulated gastric acid secretion, yet the drug had no effect on carbachol-stimulated secretion. CONCLUSIONS: S-0509 is a selective CCK-B/gastrin receptor antagonist in dogs that inhibits gastric acid secretion stimulated by pentagastrin and gastrin-releasing substances, but does not inhibit histamine-stimulated and carbachol-stimulated acid secretion.

Animals↗
PubMed1958

The pressor effect of peptone in the rat.

Peptone normally causes a rise of blood pressure in rats. Since the pressor response was not abolished or even diminished by adrenalectomy, it could not have been caused by a release of pressor substances from the adrenal glands. The group of drugs (dibenamine, dihydroergotamine, ergotamine, tolazoline, nicotine and hexamethonium) which antagonize or block the peptone-induced pressor action suggests that the pressor effect may be secondary to a release of sympathin by the stimulation of sympathetic ganglia. Since it was not possible to duplicate the pressor response to peptone by either 48/80 or histamine, the hypothesis that peptone acts by liberating histamine can be ruled out.

Adrenal Glands↗
PubMed1974

Inactivation of bacteriophage T3 in aerosols: effect of prehumidification on survival after spraying from solutions of salt, peptone, and saliva.

Coliphage T(3) was inactivated by a factor of 10(3) to 10(4) within 30 min after spraying from solutions of NaCl. Addition of peptone to the spray medium protected against inactivation at high relative humidity (RH), presumably by preventing surface inactivation. Prehumidification of the sample before collection had no effect on recovery if sprayed from solutions of NaCl, with or without peptone. If only peptone was present in the spray medium, prehumidification of the aerosol sample increased the recovery by a factor of 1,000 at low RH and by a factor of 5 at high RH. In aerosols sprayed from saliva, inactivation was nearly equal to that in peptone, with an increase of recovery after prehumidification by a factor of 1,000.

Aerosol Propellants↗
PubMed2004

Increased gastrin and calcitonin secretion after oral calcium or peptones administration in patients with hypercalciuria: a clue to an alteration in calcium-sensing receptor activity.

The calcium-sensing receptor (CaSR) has been detected in human antral gastrin-secreting cells, where, upon calcium and/or amino acid allosteric activation, it stimulates gastrin secretion. Patients with absorptive hypercalciuria (AH) display an enhanced gastric acid output; therefore, we evaluated the secretion of gastrin in subjects with AH (30 subjects vs. 30 healthy female controls, all postmenopausal) after oral calcium administration (1 g calcium gluconate) and, on a separate occasion, after peptone loading test (protein hydrolyzed, 10 g). Gastrin and monomeric calcitonin responses were higher in AH after both oral calcium administration (P < 0.01) and peptone loading (P < 0.01). Because the activation of CaSR by oral calcium and peptones directly induces gastrin release, the higher gastrin responses to these stimuli suggest an increased sensitivity of gastrin-secreting cells CaSR in patients with AH. A similar alteration in thyroid C cells might explain the enhanced calcitonin responses to both calcium and peptones. If the same alterations should in addition be present in the distal tubule (where CaSR is expressed as well), then a possible explanation for amino acid-induced hypercalciuria in AH would have been identified.

Administration, Oral↗
PubMed2006

Pork peptone stimulates cholecystokinin secretion from enteroendocrine cells and suppresses appetite in rats.

We found that soybean beta-conglycinin peptone (BconP) suppresses food intake through cholecystokinin (CCK) release from enteroendocrine cells in association with binding of the peptone to rat small intestinal brush border membrane (BBM). The aim of the present study was to find new appetite suppressing peptides. Peptones from chicken, pork, beef, beef liver, and egg white were examined for activities to bind with rat BBM, CCK-release from enteroendocrine cell line STC-1, and induce satiety in rats. Chicken and pork peptone (ChickP and PorkP) bound to BBM with highest ability as evaluated with a surface plasmon biosensor. PorkP and ChickP released CCK in higher amounts than BconP from STC-1 cells dose-dependently, with highest stimulation by PorkP. An orogastric preload of PorkP, but not ChickP, suppressed food intake similarly to BconP, dose-dependently. These results suggest that PorkP interacts directly with the small intestinal CCK cells to release CCK, and that it suppresses appetite in rats.

Animals↗
PubMed1996

[Production of free bile acids by bacterial deconjugation from conjugated bile acids derived from peptone in a medium].

In the course of studies of in vitro bile acid transformation by lactic acid bacteria, we noticed that the medium used contained conjugated bile acids. HPLC analysis of the medium for each component indicated that these bile acids had originated from a peptone (Bacto Peptone, Difco). The concentration of these bile acids in a medium containing 2% Bacto Peptone was greater than 200 microM, higher than the concentration of bile acids usually added in in vitro bile acid transformation studies. Therefore, in such studies, it would be necessary to distinguish between the production of free secondary bile acids by bacterial deconjugation and that by 7 alpha-dehydroxylation. Since bile acids affect not only bacterial growth but also many metabolic activities, particular attention should be given to the use of Bacto Peptone in the medium.

Bacteria↗
PubMed1983

Enteric release of vasoactive intestinal peptide after a peptone meal in the dog.

Vasoactive intestinal peptide (VIP) concentrations were measured by radioimmunoassay in plasma from portal and peripheral venous blood obtained from six alert, non-anesthetized dogs before and after gastric infusion of a 10% peptone meal. Mean basal portal and cephalic vein plasma VIP concentrations were 42 +/- 11.7 and 42 +/- 8.0 (S.E.M.) pg/ml, respectively. No significant changes in peripheral venous plasma VIP concentrations were noted after the peptone meal throughout the duration of the collection period. In contrast, however, the mean VIP concentration in portal plasma increased promptly after the peptone meal with a peak of 79 +/- 8.2 pg/ml (P less than 0.02) occurring 8 min after infusion of the meal. This was followed by a gradual decline in portal plasma VIP levels, with a return to prefeeding concentrations at 60 min (44 +/- 6.3 pg/ml). Results of these studies demonstrate that following gastric infusion of a peptone meal in the dog, portal, but not peripheral, plasma VIP concentrations increase significantly. Failure to detect augmentation of peripheral vein VIP levels after the meal is probably due to hepatic clearance of VIP.

Animals↗