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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↗
PubMed1988

Human preduodenal lipase is entirely of gastric fundic origin.

Lipase activity was measured in supernatant homogenates from various anatomic regions in the upper part of the human digestive tract of two organ donors. It is shown unambiguously that lipase activity occurs only in the fundic mucosa of the stomach, whereas no significant activity takes place in the antral, pharyngeal, or lingual areas, including the circumvallate papillae. In adults, the potential activity of human gastric lipase, as measured using tributyrin as substrate, amounts to 20% of its pancreatic counterpart. Lipase activity was also determined on human gastric biopsy samples taken during gastrofibroscopy tests on healthy adults. These results confirmed the finding that a lipolytic activity of gastric origin occurs uniformly and only in the fundic mucosa. Triacylglycerol hydrolysis is associated with a genuine gastric lipase activity that is clearly distinct from the classical esterase observed using p-nitrophenyl acetate as substrate. Lipase activity decreases significantly with age: it ranges on average from 4700 U/g of fresh mucosa in subjects aged up to 50 yr to 700 U/g of fresh mucosa in persons over 60 yr of age.

Adult↗
PubMed1988

Chronic obstructive pancreatitis due to tiny (0.6 to 8 mm) benign tumors obstructing pancreatic ducts: report of three cases.

Three cases of obstructive pancreatitis are described in nonalcoholic women aged 56 to 58 years with a 2-month to 5-year history of recurrent attacks of pancreatic pain associated with intermittent raised serum pancreatic enzymes. The diagnosis was made by sonography showing an enlarged hyperechogenic tail of the pancreas, with a dilated duct, the rest of the pancreas being normal, and by ERCP showing a partial stenosis of the main pancreatic duct with regular dilatation of collateral branches distally to it. Surgical resection of the pancreatic tail cured all three patients. In the obstructed part of the pancreas, the lesions are typical of obstructive pancreatitis with perilobular and sometimes intralobular fibrosis of the same degree in the different lobules of the diseased area and not patchy as in chronic calcifying pancreatitis. The changes in collateral ducts are not marked, and there is an absence of intraductal plugs. Fat necrosis and pseudocysts may be found. Tumors responsible for the obstruction were the smallest islet cell tumors (0.6 and 8 mm) and serous cystadenoma (5 mm) responsible for symptoms ever published. Cephalad to the stricture, the pancreas was normal. When the etiology of chronic pancreatitis is atypical, especially when it occurs in nonalcoholic women aged greater than 50 years, a careful sonography (or computed tomographic scan) and ERCP must be done. Serial sections of the resected pancreas at the level of the obstruction and distal to it are often necessary to demonstrate the tumor.

Adenoma, Islet Cell↗
PubMed1986

Exocrine pancreatic function of children from the Ivory Coast compared to French children. Effect of kwashiorkor.

One hundred nineteen children, either French or from the Ivory Coast, aged 1-8 years, were submitted to pancreatic function testing by duodenal aspiration. Trypsin, chymotrypsin, lipase, phospholipase, amylase, volume, bicarbonate, chloride, and calcium were estimated before and after an intravenous injection of 1 CU secretin + 3 CHR units pancreozymin per kilogram of body weight. Sixty-two patients were normal European children, and 11 were normal African children. Twenty-five African children presented with kwashiorkor and 10 African children had presented with kwashiorkor but had recovered at the time of the test. Three cases of recurrent kwashiorkor are also included. In the normal group of African children, phospholipase concentration, volume, and bicarbonate were significantly decreased but chymotrypsin and trypsin concentrations were not, when compared to the normal European population. In kwashiorkor patients, lipase, amylase, phospholipase, and chymotrypsin concentration were significantly decreased compared to normal Africans. Trypsin, volume, and bicarbonate were not affected. These modifications disappeared after refeeding. In cases of recurrent kwashiorkor, all enzymes, including trypsin, were decreased. Calcium was never modified. These modifications were very different from those observed in chronic alcoholic and hypercalcemic pancreatitis. In a two-year study, chronic calcifying pancreatitis (CCP) was diagnosed in 14 patients (13 males), hospitalized in Abidjan. The mean age at onset of the disease was 41 years (SD 12.71), which is very similar to European cases. The most frequent cause was alcoholism, as in Occidental countries. The nutrition of the population was low in protein, calories being provided mostly by manioc, but no apparent symptoms of malnutrition were observed in the parents of our patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

Action of pirenzepine, a new muscarinic antagonist drug, on human pancreatic secretion.

The action of a new muscarinic antagonist drug on the pancreatic secretion has been studied in 12 healthy subjects. A stable pancreatic secretory plateau was obtained with submaximal hormonal stimulation (0.125 CU/kg/h secretin: 30 ng/kg/h caerulein). The highest dose of pirenzepine (40 mg) inhibited both volume and enzymatic concentration and output (-72.2% and -77.9% of plateau value for chymotrypsin and lipase output, respectively, 30 min after pirenzepine injection). The inhibition appeared immediately, lasted for more than 60 min, and was dose-related. The calcium dose-response curve paralleled those of lipase and chymotrypsin outputs. These results were comparable to those obtained with other anti-acetylcholine drugs and may be associated with the action of certain doses of ethanol on pancreatic secretion. In contrast, the lowest pirenzepine dose used (10 mg) induced a delayed stimulation of bicarbonate output, and bicarbonate concentration was not altered.

Adult↗
PubMed1985

Alcohol and the integrity of the pancreas.

Alcohol may affect the integrity of the pancreatic parenchyma, as seen in alcoholic pancreatitis, some cases of chronic alcoholism without clinical pancreatitis, and experimental studies. The composition of pancreatic juice may reflect some of these changes. One type of parenchymal alteration is the loss of differentiative features of acinar cells, so that they take on the characteristics of ductular cells. Concomitant fibrosis completes the formation of the tubular complexes found in association with alcoholic chronic pancreatitis. Sustained alcohol intake may produce the accumulation of lipid droplets in parenchymal cells, some of which may be shown to be within the rough endoplasmic reticulum of acinar cells. Epithelial cells may undergo mucous metaplasia. The epithelial-basal lamina barrier frequently is breached in the area of intraluminal aggregates, with or without obvious inflammation in the immediate area. Loss of barrier function may lead to interaction among components of the external compartment (lumen) and the internal compartment (stroma). Increased levels of blood proteins and glycosaminoglycans in the juice, enzyme activation, fibrin formation, and complement activation are potential consequences of barrier loss. Increased lactoferrin levels could result in part from the activity and degranulation of polymorphonuclear leukocytes.

Alcoholism↗