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G Gomez

Publications and source records attributed to G Gomez.

At least 91 records · Page 5Linked to original sources
PubMed1989

Evidence for regulation of peptide-YY release by the proximal gut.

Peptide-YY (PYY) is a novel enteric peptide that is structurally related to pancreatic polypeptide and neuropeptide-Y. The objectives of the present experiments were to characterize the following aspects of PYY metabolism: the distribution of PYY in the canine gastrointestinal tract, the release of PYY in response to oral ingestion of a mixed meal or intraduodenal (ID) administration of oleic acid, the effect of ileocolectomy on the release of PYY in response to ID administration of oleic acid when transit of chyme to the distal ileum and colon is prevented, the effect of interruption of intramural neural pathways of the small bowel on the release of PYY, and the effect of iv cholecystokinin on the release of PYY. The results of these experiments demonstrate that PYY immunoreactivity is distributed primarily in the terminal ileum, colon, and rectum. Circulating levels of PYY increase significantly (P less than 0.05) within 10-30 min after ingestion of a meal or to ID administration of a fatty acid. Complete interruption of the flow of chyme to the site of PYY-containing cells (i.e. ileum-colon) did not block the release of PYY; however, ileocolectomy abolished the release of PYY in response to ID administration of oleic acid. Severance of intramural neural pathways along the small bowel did not alter the release of PYY in response to an oral meal. Intravenous administration of graded doses of cholecystokinin stimulated the release of PYY in a dose-related manner. The results of these experiments indicate that the release of PYY from the distal ileum and colon is controlled, at least in part, by an extramural neural, endocrine, or a combination of both types of mechanisms which originate in the foregut.

Animals↗
PubMed1989

A comparison of intraduodenally and intracolonically administered nutrients on the release of peptide-YY in the dog.

The objective of this study was to compare the effects of various nutrients (fats, proteins, amino acids, and carbohydrates), given directly into the duodenum or the colon, on the release of peptide-YY (PYY) in conscious dogs. As reported previously, this study showed that plasma levels of PYY increased significantly (P less than 0.05) within 15 min in response to an oral mixed meal. Intraduodenal (ID) administration of a fatty acid (oleic acid; 100 mmol/L; 100 ml/h) stimulated a robust release of PYY, whereas ID administration of an amino acid mixture (phenylalanine plus tryptophan; 100 mmol/L each; 100 ml/h), glucose (1 g/kg), or a liver extract (10%; 100 ml/h) failed to elevate plasma levels of PYY. ID administration of glucose at 2 g/kg caused a mild but significant elevation in plasma PYY levels. Intracolonic administration of saline, a fatty acid, an amino acid mixture, glucose, or a liver extract significantly stimulated PYY release. This study suggests that as chyme moves from the stomach to the proximal bowel, fat is the primary constituent of food that stimulates the prompt release of PYY. However, unabsorbed nutrients can release PYY by a direct contact with the PYY-containing cells lining the intestinal lumen of the terminal ileum, colon, and rectum. Both mechanisms probably participate in the release of PYY.

Amino Acids↗
PubMed1989

Involvement of cholecystokinin receptors in the adverse effect of glucocorticoids on diet-induced necrotizing pancreatitis.

The mechanism that explains the association between corticoids and acute pancreatitis is unknown. Our hypothesis was that chronic glucocorticoid treatment could adversely affect the course of hemorrhagic pancreatitis by acting through cholecystokinin (CCK) receptors. Acute necrotizing pancreatitis was induced by feeding young female mice a choline-deficient, ethionine-supplemented (CDE) diet for 60 hours. Treatment with hydrocortisone (10 mg/kg/day) was begun 1 week before pancreatitis. At the onset of the CDE diet, a group of hydrocortisone-treated mice were also given the CCK receptor antagonist CR-1409 (5 mg/kg three times a day). Control mice received injections of saline solution. A follow-up of 336 hours was conducted for survival analysis. Hydrocortisone given alone did not produce pancreatitis. Hydrocortisone, however, did increase the pancreatic necrosis caused by the CDE diet (from 40% to 70%) and significantly reduce survival (from 40% to 9%). CR-1409 completely abolished the adverse effects of hydrocortisone on pancreatitis. We measured amylase release by dispersed pancreatic acini from mice chronically treated with hydrocortisone in response to CCK-8. Treatment with hydrocortisone increased both the sensitivity and the responsiveness of the pancreas to CCK-8. We conclude that glucocorticoids alone may not induce acute pancreatitis, but they can increase the risk of a more severe form of pancreatitis developing. The glucocorticoid effect appears to be attributable to a CCK receptor-mediated sensitization of the pancreas to endogenous CCK. Thus, CCK-receptor blockade may improve survival in necrotizing pancreatitis associated with chronic glucocorticoid treatments.

Amylases↗
PubMed1989

Retrohepatic vein injuries: experience with 20 cases.

The mortality for injury of the retrohepatic veins is reported to vary from 50 to 100%. The use of hepatic bypass techniques, introduced in the 1960's, has not significantly decreased this mortality. We reviewed our experience with liver injuries over a 5-year period from 1982 to 1987 to determine our results with these particular injuries. Twenty patients had retrohepatic vein injuries. There were 11 patients with penetrating trauma and nine with blunt trauma. A total of 15 patients died, for a mortality rate of 75%. Fourteen patients died intraoperatively from exsanguination and one postoperatively from sepsis. A shunt was used in an attempt to bypass the injury in ten patients, with nine deaths. In the ten remaining patients who were not shunted, there were six deaths. Thus, in ten shunted patients the mortality was 90% and in ten non-shunted patients, 60%. Our review supports other studies reporting a lower mortality by direct exposure and repair of retrohepatic vein injuries. Although total vascular occlusion of the liver may not be well tolerated in hypotensive patients, rapid application of the above approach resulted in better patient survival than the use of shunts.

Adult↗
PubMed1989

Gastrointestinal peptides.

The intent of this article is to summarize the primary structures (that is, amino acid sequences) localization, primary gastrointestinal and pancreatic actions, and possible clinical relevance of the major gut peptides as well as some of the miscellaneous gut peptides. A brief overview of the general characteristics of gut peptides is presented.

Digestive System Physiological Phenomena↗
PubMed1988

Structure of cis-Pt(asb)2Cl2, a platinum(II) complex with a styrylbenzothiazole ligand.

cis-Bis[2-(2-acetoxystyryl)benzothiazole]dichloroplatinum(II), [PtCl2(C17H13NO2S)2], Mr = 856.7, triclinic, P1, a = 12.145 (6), b = 12.859 (4), c = 11.021 (5) A, alpha = 105.88 (3), beta = 90.64 (4), gamma = 87.64 (4) degrees, V = 1654 (2) A3, Z = 2, D chi = 1.72 g cm-3, lambda(Mo K alpha) = 0.71073 A, mu = 46.1 cm-1, F(000) = 840, T = 296 K, final R = 0.029 for 6121 unique observed reflections. The [PtCl2(asb)2] complex has square-planar geometry about the Pt, with the asb coordinated to the Pt through the N of the thiazole ring. The average Pt-N and Pt-Cl bond distances are 2.035 (1) and 2.287 (5) A. The ligand is non-planar with an average dihedral angle of 36 (3) degrees between the benzothiazole and the benzene rings. The dihedral angles between the platinum coordination plane and the benzothiazole and benzene rings are 78 (4) and 69 (7) degrees respectively. The acetoxybenzene rings in the two ligands have different orientations with respect to the olefin C atoms.

Antineoplastic Agents↗
PubMed1988

Regulation of the release of cholecystokinin by bile salts in dogs and humans.

The objective of these studies was to investigate the role of bile salts in the regulation of release of cholecystokinin in response to nutrients in dogs and humans. In dogs, the intraduodenal administration of a bile salt sequestrant, cholestyramine (2, 4, or 8 g/h), resulted in a dose-related enhancement of the release of cholecystokinin-33/39 and pancreatic protein secretion in response to intraduodenal administration of amino acids. Intraduodenal administration of cholestyramine alone did not affect basal levels of cholecystokinin-33/39 or pancreatic protein secretion. Total diversion of bile also significantly increased the release of cholecystokinin and pancreatic protein secretion in response to intraduodenal administration of amino acids. Replacement of the bile salt pool by intraduodenal administration of taurocholate completely reversed the enhancement effect of both cholestyramine and bile diversion. In humans, oral ingestion of cholestyramine (12 g) significantly increased the release of cholecystokinin-33/39 and gallbladder contraction in response to the oral ingestion of either a triglyceride or amino acids. These results support a physiologic role of bile salts in the negative feedback regulation of release of cholecystokinin in response to luminal nutrients.

Adult↗
PubMed1988

Peptide YY inhibits pancreatic secretion by inhibiting cholecystokinin release in the dog.

Peptide YY inhibits the pancreatic exocrine secretion (bicarbonate, water, and protein) that is stimulated by cholecystokinin, secretin, or neurotensin in the dog, but whether peptide YY inhibits the release of gut peptides that stimulate pancreatic exocrine secretion is not known. Six dogs were prepared with gastric, pancreatic, and cecal cannulas. On separate days, a single dose of sodium oleate (3, 6, 7.5, 9, 12, 15, or 18 mmol/h) was given intraduodenally for 90 min, either alone (control) or in combination with peptide YY (25, 50, 100, 200, or 400 pmol/kg.h, i.v.). We measured plasma levels of cholecystokinin-33/39, secretin, neurotensin, and peptide YY by radioimmunoassay. During infusion of peptide YY, the integrated release of cholecystokinin (3.3 +/- 0.5 ng-[0-90] min/ml) was decreased significantly (p less than 0.05) when compared with control values (5.6 +/- 0.6). Release of secretin and neurotensin was not affected. A positive correlation (p less than 0.05) was found between the release of cholecystokinin and pancreatic protein output in both control (r = 0.68) and peptide YY-treated (r = 0.67) groups. Release of peptide YY was significant after intraduodenal or intracolonic administration of sodium oleate. These studies demonstrate that inhibition of pancreatic protein secretion by peptide YY in dogs is mediated, at least in part, by an inhibition of the release of cholecystokinin.

Animals↗
PubMed1988

Peptide YY and gallbladder contraction. Studies in vivo and in vitro.

The purpose of this study was to examine the effect of peptide YY on contraction of the gallbladder in vivo and in vitro and on contraction of the sphincter of Oddi in vitro. In conscious dogs that were prepared with strain-gauge force transducers implanted in the gallbladder wall, peptide YY (400 ng/kg, bolus; 800 pmol/kg.h, infusion) did not affect the resting contractile pattern of the gallbladder, nor did it inhibit cholecystokinin-octapeptide (CCK-8)-stimulated gallbladder contraction. In contrast, the cholecystokinin antagonist proglumide (5, 10, 20, 40, or 80 mg/kg), given in vivo, inhibited CCK-8-stimulated gallbladder contraction in a dose-related manner. The highest dose of proglumide (80 mg/kg) completely abolished contraction of the gallbladder stimulated by CCK-8. In vitro studies showed that peptide YY (0.25, 0.5, or 1 microgram/ml) did not affect the resting tension of rabbit gallbladder strips, and it did not inhibit CCK-8-stimulated contraction of gallbladder strips. Proglumide (0.4, 0.8, 1.6, or 3.2 mg/ml) inhibited CCK-8-stimulated tension of gallbladder strips in a dose-related manner. Peptide YY and CCK-8 had no effect on the motility of the canine sphincter of Oddi in vitro, whereas acetylcholine caused contraction and adrenergic agonists caused relaxation. These results suggest that peptide YY and pancreatone (a peptidelike substance, extracted from ileal and colonic mucosa, that inhibits CCK-8-stimulated gallbladder contraction in vivo) do not appear to be identical.

Ampulla of Vater↗
PubMed1988

Peptide YY antagonizes beta-adrenergic-stimulated release of insulin in dogs.

Peptide YY (PYY) and neuropeptide Y (NPY) are peptides of 36 amino acids that share structural homologies with pancreatic polypeptide (PP). PP is predominantly found in the endocrine pancreas. PPY is primarily found in mucosal endocrine cells of the distal ileum, colon, and rectum, whereas NPY is found in both the peripheral and central nervous systems. Previous studies indicate that these peptides can interact with the autonomic nervous system. The objective of the present experiments was to study the effect of PYY on neurally stimulated insulin release [i.e., in response to 2-deoxy-D-glucose (2-DG), a nonmetabolizable glucose analogue] in conscious dogs. Intravenous administration of PYY (100, 200, and 400 pmol.kg-1.h-1) reduced 2-DG-stimulated insulin release in a dose-dependent manner (P less than 0.05) without affecting plasma glucose levels. Administration of NPY (800 pmol.kg-1.h-1), but not PP (400 pmol.kg-1.h-1), reduced 2-DG-stimulated release of insulin (P less than 0.05). The inhibitory action of PYY on 2-DG-stimulated insulin release persisted in the presence of atropine or phentolamine treatment; however, hexamethonium alone or phentolamine plus propranolol treatment blocked the inhibitory action of PYY. Release of insulin stimulated by the beta-agonist isoproterenol was also inhibited by PYY (P less than 0.05). These results indicate that PYY can inhibit autonomic neurotransmission by a mechanism that may involve ganglionic or postganglionic inhibition of beta-adrenergic stimulation. Our findings suggest a role for PYY and NPY in the autonomic regulation of insulin release.

Animals↗
PubMed1988

Inhibition of gastric acid secretion by peptide YY is independent of gastric somatostatin release in the rat.

The purpose of this study was to determine whether the inhibitory action of peptide YY (PYY) on gastric acid secretion is attributable to the release of gastric somatostatin in rats. Two groups of rats (six rats/group) were anesthetized with urethane and prepared with gastric fistulas and jugular catheters. Pentagastrin (18 micrograms/kg-h) was given intravenously for 150 min to stimulate gastric acid secretion. Intravenous PYY (130 micrograms/kg-h) inhibited pentagastrin-stimulated gastric acid secretion significantly (P less than 0.05). Administration of iv PYY resulted in a 41% reduction (P less than 0.05) in pentagastrin-stimulated gastric acid secretion. In another group of anesthetized rats, administration of PYY (10(-7), 10(-8) M) failed to stimulate a release of somatostatin from the isolated-perfused rat stomach. Our findings indicate that PYY can inhibit gastric acid secretion independently of release of gastric somatostatin in the rat.

Animals↗
PubMed1987

Peptide YY interacts with secretin and duodenal acidification to inhibit gastric acid secretion.

Previous studies have indicated that plasma levels of peptide YY (PYY) increase significantly after a meal. The purpose of this study was to characterize the interaction of PYY and secretin in the inhibition of gastric acid secretion, and to determine whether PYY can influence acid-induced inhibition of gastric acid secretion in conscious dogs. I.v. administration of PYY at 200 pmol/kg/h inhibited pentagastrin (1 microgram/kg/h)-stimulated gastric acid output (P less than 0.05). PYY further augmented i.v. secretin-induced inhibition of pentagastrin-stimulated gastric acid output by 32 +/- 7%, and intraduodenal hydrochloric acid-induced inhibition of pentagastrin-stimulated gastric acid output by 40 +/- 12%. The mean integrated release of secretin response to duodenal acidification (3.9 +/- 1.0 ng-[0-60] min/ml) was not affected by PYY (3.3 +/- 0.9 ng-[0-60] min/ml). The present study demonstrates that PYY can interact with secretin and duodenal acidification in an additive fashion to inhibit pentagastrin-stimulated gastric acid secretion. Our results suggest that several hormones that are released postprandially can interact with each other to inhibit gastric acid secretion.

Animals↗
PubMed1987

Effect of peptide YY on cephalic, gastric, and intestinal phases of gastric acid secretion and on the release of gastrointestinal hormones.

The objective of this study was to investigate the effects of a novel gut peptide, peptide YY (PYY), on the cephalic, gastric, and intestinal phases of gastric acid secretion and to explore the mechanisms involved. The cephalic phase of gastric acid secretion, stimulated by the intravenous injection of 2-deoxyglucose (75 mg/kg), was found to be inhibited by intravenous PYY (100, 200, 400 pmol/kg X h) in a dose-related fashion. Peptide YY (200 and 400 pmol/kg X h) also resulted in a significant dose-dependent inhibition of the gastric phase of acid secretion. On the other hand, PYY (400 pmol/kg X h) failed to affect the intestinal phase of gastric acid output. Serum gastrin levels were increased on infusion of 10% liver extract into stomach, but were unaffected on instillation of liver extract into duodenum. Peptide YY did not inhibit the release of gastrin in either the gastric or intestinal phase studies. Furthermore, PYY had no significant effect on either the basal release of secretin, gastric inhibitory polypeptide, pancreatic polypeptide, or neurotensin, or on the stimulated release of pancreatic polypeptide by 2-deoxyglucose. The specific binding of gastrin to its receptors on the fundic mucosa was also unaffected by PYY. These results indicate that PYY inhibits the cephalic and gastric phases of acid secretion independently, and that its actions are not mediated by either a negative effect on gastrin release or a positive effect on the release of some of the known acid inhibitors, or by an inhibition of gastrin binding to its receptors on the fundic cells. Our present findings (in combination with our previous findings of inhibition of pentagastrin- and bethanechol-stimulated gastric acid secretion by PYY, independent of the vagal cholinergic mechanism) indicate that the action of PYY is either direct on the parietal cells or is mediated by yet another, unidentified, inhibitor.

Animals↗
PubMed1987

Peptide YY inhibits nutrient-, hormonal-, and vagally-stimulated pancreatic exocrine secretion.

Peptide YY (PYY) is a recently isolated gut peptide that is found primarily in the mucosal endocrine cells of the terminal ileum, colon, and rectum of several mammalian species, including humans. The purpose of this study was to characterize the effect of PYY on pancreatic exocrine secretion in six conscious dogs prepared with pancreatic and gastric fistulas. In control experiments, pancreatic exocrine secretion was stimulated by either intravenous (i.v.) administration of secretin (100 ng/kg/h), cholecystokinin-8 (50 ng/kg/h), neurotensin (5 micrograms/kg/h), or 2-deoxy-D-glucose (75 mg/kg); or by the intraduodenal infusion of hydrochloric acid (4 mEq/h), a mixture of amino acids (phenylalanine + tryptophan at 5 mmol/h), sodium oleate (9 mmol/h), or a liquid meal. On separate days, PYY (12.5, 25, 50, 100, 200, or 400 pmol/kg/h) was given intravenously in combination with one of the above pancreatic secretagogues. Intravenous PYY at 200 and 400 pmol/kg/h inhibited secretin-stimulated pancreatic bicarbonate output significantly (p less than 0.05). Pancreatic bicarbonate and protein responses to all pancreatic secretagogues were reduced significantly (p less than 0.05) by PYY at 400 pmol/kg/h. Intravenous administration of atropine (0.6 mg bolus, followed by 0.02 mg/kg/h) did not abolish the ability of PYY to inhibit secretin-stimulated pancreatic bicarbonate secretion. This study demonstrates that PYY can inhibit nutrient-, hormonal-, and vagally-stimulated pancreatic exocrine secretion in the dog; its mechanism of action appears to be independent of cholinergic innervation.

Amino Acids↗
PubMed1987

Effects of the addition of vegetable oil or animal tallow to broiler diets containing cassava root meal.

Two experiments were carried out to evaluate the effects on broiler performance of increasing by 5% the metabolizable energy level of diets containing cassava (Manihot esculenta Crantz) root meal (CRM: 0, 20, and 30%) by adding either vegetable oil (Experiment 1) or animal tallow (Experiment 2). The CRM used was detoxified by sun-drying whole root chips of a high cyanide-containing (bitter) cultivar (CMC-84) on a concrete floor. All experimental diets were supplied in mash form. Supplementary vegetable oil or animal tallow did not affect (P greater than .05) growth rate. Feed conversion (feed/gain) was improved (P less than .05) during the starter (0 to 28 days) period as well as at the end of the experiments (56 days). Body weight gain, feed consumption, and feed conversion were not affected (P greater than .05) by any of the dietary treatments during the finishing (28 to 56 days) period of both experiments. Diets containing 20% CRM produced somewhat higher (P greater than .05; Experiment 1) or significantly higher (P less than .05, Experiment 2) final body weights.

Animal Feed↗
PubMed1987

Bile enhances release of insulin: an incretin-mediated effect.

Ingestion of food stimulates secretion of bile and release of gut hormones that enhance nutrient-stimulated release of insulin. The extent of physiologic participation of bile in the enteroinsular axis was examined in seven conscious dogs (weight: 20 +/- 2 kg) that were prepared for study with chronic cannulas placed in the duodenum opposite the ampulla of Vater. On separate days, a meal consisting of 10 gm (MG-10), 25 gm (MG-25), or 62 gm (MG-62) of glucose (dextrose) was given orally in the presence of normal bile flow or during bile diversion. Bile diversion was achieved by catheterization of the common bile duct via the duodenal cannula. The insulin responses (given as ng [0-120] min/ml) to the different glucose meals, with bile present (BP) or absent (BA) in the lumen, were as follows: MG-10, 81 +/- 8 BP and 72 +/- 11 BA; MG-25, 172 +/- 25 BP and 100 +/- 6 BA (p less than 0.05); and MG-62, 390 +/- 79 BP and 153 +/- 32 BA (p less than 0.05). Only MG-25 and MG-62 produced a significant elevation of plasma glucose concentrations. Release of gastrin was not affected by either the presence of bile or the glucose content of the meal. We conclude that endogenous bile enhances nutrient-stimulated release of insulin, this effect is glucose-dependent with a threshold of approximately 1 gm/kg of glucose, and bile may facilitate the release of insulinotropic hormones other than gastrin.

Animals↗
PubMed1986

Effect of cyanogenic glycosides and protein content in cassava diets on hamster prenatal development.

Cassava is a staple food for 450-500 million people in 26 tropical countries. Groups of pregnant hamsters were fed diets consisting of cassava meal:laboratory chow (80:20) during Days 3-14 of gestation. One low cyanide (sweet) cassava meal and one high cyanide (bitter) cassava meal were studied. One additional group was fed a diet which resembled cassava in nutritional value, but which lacked the cyanogenic glycosides. Thiocyanate concentrations increased significantly in the urine and blood of dams fed cassava diets. Increased tissue thiocyanate concentrations were observed in fetuses recovered from cassava-fed dams. Cassava-fed dams gained significantly less weight than did control animals and their offspring showed evidence of fetotoxicity. Reduced fetal body weight and reduced ossification of sacrocaudal vertebrae, metatarsals, and sternebrae were associated with cassava diets. High cyanide cassava diets were also associated with a significant increase in the numbers of runts compared to litters from dams fed either low protein or laboratory stock diets.

Animals↗