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Biomedical subjects

R Laugier

Publications and source records attributed to R Laugier.

At least 19 recordsLinked to original sources
PubMed1992

Dog gastric lipase: stimulation of its secretion in vivo and cytolocalization in mucous pit cells.

Dog gastric lipase (DGL) secretion is stimulated in vivo by urecholine, pentagastrin, histamine, 16,16-dimethyl prostaglandin E2, and secretin. Under fasting conditions, DGL is irreversibly inactivated by gastric acid below pH 1.5; consequently, DGL output can be underestimated. This problem has been resolved by buffering the acid or by using an antisecretory drug such as omeprazole during stimulation. There is a clear parallelism between the secretion of DGL and of gastric mucus. This observation led to the present investigation of the cellular localization of DGL using immunofluorescence techniques. Results showed that DGL is cytolocalized in mucous pit cells of gastric glands. Pepsinogen is found in chief cells. To the authors' knowledge, this is the first description of an enzyme (gastric lipase) secreted by mucous-type gastric cells. In contrast to other species, gastric lipase of the dog is located in cardiac, fundic, and antral mucosae.

Animals↗
PubMed1991

Purification and biochemical characterization of dog gastric lipase.

A lipase was found to be present in dog stomach which appeared to be more abundant in the fundic than in the pyloric mucosa. Dog gastric lipase was extracted by soaking the gastric tissue and further purified after cation exchange, anion exchange and gel-filtration using fast protein liquid chromatography. The amino-acid composition, N-terminal amino-acid sequence, substrate specificity, interfacial and kinetic behavior and inactivation by sulfhydryl reagents were determined and compared with those of human and rabbit gastric lipases. We report for the first time that a gastric lipase is 13 times more active on long-chain than on short-chain triacylglycerols at pH 4.0, reaching a maximal specific activity of 950 U/mg on Intralipide emulsion.

Amino Acid Sequence↗
PubMed1991

CCK and PYY do not participate in the delayed inhibition of pancreatic secretion, after stimulation by duodenal oleic acid infusion.

The role played by CCK in the stimulation of pancreatic secretion by duodenal infusion of oleic acid in conscious rats was studied using a potent and specific CCK receptor antagonist. CR-1409 did not alter basal secretion, which does not require CCK. The three doses of CR-1409 that were used (2, 4 and 8 mg/kg/h) suppressed the protein response to duodenal infusion of oleic acid and significantly enhanced the delayed inhibition normally observed in control rats (-81%, -87% and -88% vs. -51% of basal in controls). CR-1409 dose-dependently reduced the volume of pancreatic secretion after duodenal infusion of oleic acid (0.40 +/- 0.02, 0.36 +/- 0.02, 0.34 +/- 0.03 vs. 0.48 +/- 0.04 ml/30 min for 2, 4, 8 mg/kg/h and controls, respectively) and revealed a delayed inhibition of volume and a slight reduction of bicarbonate secretion. CCK appears to be directly responsible for the protein and also water response to duodenal infusion of oleic acid, and to be indirectly involved in bicarbonate stimulation. PYY antiserum significantly augmented protein output after duodenal infusion of oleic acid (10.75 +/- 1.40, 14.10 +/- 1.60 vs. 8.60 +/- 1.20 mg/30 min, 1 microliter, 2 microliters and controls), but failed to modify the delayed inhibition: PYY modulates the response to duodenal infusion of oleic acid and is not involved in the delayed inhibition, which was shown to be also present for volume, but which is normally masked by the action of CCK.

Animals↗
PubMed1991

Effects of zinc and copper deficiency associated with protein or lipid deficiency on rat exocrine pancreatic secretion.

Copper and zinc are both secreted by the pancreas but are necessary for pancreatic secretion. We have studied the effects of a 4- or 8-week zinc or copper-deficient diet associated with or without lipid or protein deficiency on rat pancreatic secretion after stimulation by secretin, cerulein, or intraduodenal oleic acid. Twenty animals were in the control group; 40 rats were fed a copper-deficient diet (20 copper-deficient only and 20 copper- plus lipid-deficient). Ninety rats were deprived of zinc (30 of zinc-deficient only, 30 zinc-plus protein-deficient, 30 of zinc- plus lipid-deficient). Only the zinc- plus lipid-deficient diet for 8 weeks decreased basal bicarbonate and basal protein secretion (-42 and -70%, respectively, of the control values). Stimulated secretion was not markedly altered by copper deficiency while zinc deficiency, zinc plus protein deficiencies, and zinc plus lipid deficiencies suppressed almost responses to hormonal stimulation: After 8 weeks, the maximal protein response to oleic acid was reduced to 19.00 +/- 3.40, 18.58 +/- 3.00, and 12.04 +/- 2.91 microgram/30 min/g body weight in zinc- zinc and protein-; and zinc- and lipid-deficient diet, respectively, versus 39.87 +/- 6.33 microgram/30 min/g body weight (p less than 0.05) in controls. In all types of stimulation, lipid deficiency potentiated the deleterious effect of zinc deficiency on pancreatic secretion. This might be paralled with an extremely low level of lipid in the diet of people living in countries in which nutritional pancreatitis is observed and with the relative risk of developing an alcoholic chronic pancreatitis being increased by a low fat diet.

Animals↗
PubMed1991

Changes in pancreatic exocrine secretion with age: pancreatic exocrine secretion does decrease in the elderly.

Pancreatic exocrine secretion was estimated in 180 normal control patients, free of abdominal and pancreatic disease, aged from 16 to 83 years. Duodenal juice was collected in two 15-min fractions after a single intravenous injection of 1 U/kg secretin + 3 U/kg CCK. Volume, maximal concentration and output of bicarbonate, lipase, phospholipase and chymotrypsin were estimated as well as minimal concentration and output of chloride and calcium. Each parameter was plotted against age, either individually or after separation into two age groups. Volume linearly increased up to the 3rd decade, and thereafter linearly decreased. Bicarbonate secretion paralleled fluid secretion and also decreased after the 3rd decade. The changes in chloride and calcium concentrations were different: concentrations linearly increased after the 3rd decade. Calcium concentration linearly increased with age (p less than 0.02) while chloride output was unchanged. The three enzymes that were studied linearly decreased in concentration as well as in output with age from the 3rd decade (p less than 0.02). Protein secretion decreased before water and bicarbonate secretion. One can conclude that pancreatic secretion changes in humans with age. Aging alters pancreatic secretion, through a decrease in flow rate, bicarbonate and enzyme secretion while calcium concentration is enhanced. Although not requiring substitutive therapy in the whole population, individual cases of pancreatic exocrine insufficiency might be explained by aging, without malnutrition.

Adult↗
PubMed1989

Immunocytolocalization of human gastric lipase in chief cells of the fundic mucosa.

The presence in human gastric juice of a lipase secreted by the gastric mucosae has been reported previously, but its exact cellular origin has not yet been established. Polyclonal antibodies specific to human gastric lipase (HGL) were prepared, and used by an immunofluorescence technique to label cells producing HGL. This immunocytolocalization was correlated with that of pepsin (chief cells) and parietal cells using specific polyclonal or monoclonal antibodies. Our results clearly establish that HGL is exclusively located in the chief cells of fundic mucosa; furthermore, it was found to be always co-located with pepsin. No HGL was observed in the parietal or mucus cells. HGL was always detected intracellularly, either in secretory granules of the apical region of the chief cells, or revealed by more diffuse cytoplasmic labelling.

Antibodies↗
PubMed1986

Dopamine, noradrenaline and isoprenaline: secretory and electrophysiological effects in vitro on mouse pancreas.

The amylase release from mouse pancreatic fragments was studied after dopamine (DA), and alpha- or beta-sympathomimetic agonist application. The electrical parameters of the acinar cell membrane were also monitored. Both DA (from 5 X 10(-6) to 10(-4) M) and beta-stimulants (isoprenaline from 5 X 10(-6) to 5 X 10(-5) M; noradrenaline from 3 X 10(-4) to 10(-3) M) evoked an increase in amylase release, while noradrenaline in alpha-receptor stimulating doses failed to have any effect. The stimulatory effect of DA was blocked by ganglion blockers (Arfonad 10(-5) M; pentamethonium 3 X 10(-5) M) in a competitive manner and a dual antagonism was observed with atropine (10(-7) M, 10(-9) M). An alpha-receptor antagonist (phentolamine 10(-5) M) and a beta-receptor antagonist (propranolol 10(-5) M) had no influence on the dopamine response. Moreover, the DA-induced stimulation was dependent on the presence of extracellular calcium. Perfusion with 10(-4) and 10(-3) M-DA or local application (from 77 micrograms to 4.3 mg), resulted in marked membrane depolarization with diminution of the input resistance. This effect was blocked by atropine (10(-5) M) and pentamethonium (10(-4) M), but not by propranolol (10(-5) M) or phentolamine (10(-5) M). The isoprenaline- (IP) and noradrenaline- (NA) induced increase in amylase release was competitively blocked by propranolol (10(-5) M) but not by phentolamine (10(-5) M). Atropine caused a dose-dependent (10(-7) M, 10(-6) M) decrease in the maximal response (non-competitive antagonism), while the ganglion blocker pentamethonium (10(-4) M) was without effect. NA caused membrane depolarization accompanied by a decrease in the input resistance after local application (from 77 micrograms to 1.6 mg). This effect persisted in the presence of 10(-5) M-phentolamine but was abolished by 10(-5) M-propranolol. IP perfusion (10(-4) and 10(-3) M) or local application (0.3 M; from 32 to 130 micrograms) caused the same electrical changes as those induced by NA and DA. The effect of IP persisted in the presence of 10(-5) M-phentolamine, 10(-4) M-pentamethonium and 10(-4) M-domperidone, but was abolished by propranolol (10(-5) M) and tetrodotoxin (5 X 10(-6) M) and markedly diminished by atropine (10(-5) M).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

The pancreas.

Explore the source record for details and available documents.

Adenocarcinoma↗
PubMed1979

Pancreatic response to secretion+CCK-PZ in European and North African adults and children.

Pancreatic response to intravenous secretin GIH (1CU/kg) +CCK-PZ (3CHRU/kg) was investigated in European and North African normal subjects. The pancreatic responses were compared in two groups of 38 normal male adults and in two groups of nine normal nurslings (less than 1 year). Body weight and age were similar in the two adult groups and in the two nursling groups. The peaks of volume, electrolytes, and enzymes were determined in samples of duodenal aspirate after hormonal stimulation. In adult subjects the flow rate and electrolytes were not statistically different in the two groups, while enzyme outputs were lower in the North African group -73% for lipase (P less than 0.001), -54% for phospholipase (P less than 0.01), and -35% for chymotrypsin (P less than 0.05). On the other hand, in both groups of nursling subjects all parameters of pancreatic secretion were identical. The difference in the pattern of the pancreatic response to exogenous hormonal stimulation observed between the two groups of adult subjects could be related to genetic or acquired differences. The second hypothesis is, however, the most probable because the pancreatic secretion was similar in both groups of nursling subjects.

Adult↗
PubMed1979

Inhibition of rat pancreatic secretion by neurotensin: mechanism of action.

The effect of neurotensin on rat pancreatic secretion was studied in the conscious animal as well as on pancreatic lobules. In vivo neurotensin induced a dose-related inhibition of both water and protein basal secretion. Protein secretion was much more depressed than fluid secretion. Neurotensin did not modify the pancreatic response to exogenous secretin or cholecystokinin-pancreozymin, or to intraduodenal infusion of HCl. On the other hand neurotensin totally inhibited the increase in volume as well as in protein output to an intraduodenal infusion of oleic acid, but did not change the delayed inhibitory effect on protein output. In vitro, neurotensin did not affect basal and cholecystokinin stimulated pancreatic secretion. These results indicate that: 1) neurotensin could interfere with the release of hormones from the gut (cholecystokinin, and possibly VIP), 2) neurotensin did not mimic the delayed protein inhibitory effect observed after administration of oleic acid.

Amylases↗
PubMed1977

Action of oleic acid on the exocrine pancreatic secretion of the conscious rat: evidence for an anti-cholecystokinin-pancreozymin factor.

The effects on exocrine pancreatic secretion of an intraduodenal infusion of oleic acid (2 ml in 60 min) has been assessed in conscious rats provided with a new type of duodenal cannula permitting the normal flow of pancreatic juice, but not of bile, between experiments.1. Intraduodenal oleic acid infusion induces an increased secretion of water and bicarbonate which is still significantly above basal values 90 min after the end of infusion. Protein output increased during the infusion, but protein concentration and output significantly decreased under basal levels 120 min and 150 min after infusion (respectively -63 and -57% of basal values at 150 min).2. No inhibition was found when oleic acid was introduced into the caecum or into the first 20 cm of ileum isolated from the rest of small intestine. On the contrary, inhibition of protein secretion was induced immediately by intra-ileal oleic acid infusion.3. Inhibition of protein secretion secondary to intra-ileal oleic acid infusion was transmitted from a donor rat to a receiver rat by means of a cross-circulation.4. It is concluded that oleic acid induces an immediate and long lasting increase in water and bicarbonate secretion. During the infusion of oleic acid, protein output is increased, followed by an inhibition. This delayed inhibition stems from the second part of the small intestine and was transferred from one rat to another by cross-circulation: it is speculated that oleic acid releases in the conscious rat (from the distal part of the small intestine) a hormonal factor inhibiting pancreatic secretion.

Animals↗