Variação aniônica da dieta sobre características ósseas de frangos de corte: resistência à quebra, composição orgânica e mineral / Diet anionic variation in the broiler chick bone: breaking force resistance, organic and mineral composition

Avaliou-se a composição química e a resistência óssea do tibiotarso de frangos de corte aos 21 dias de idade. Foram determinados os percentuais ósseos de proteínas colagenosas (PC) e proteínas não colagenosas (PNC) e de cálcio, fósforo, potássio e sódio. Foram utilizados 650 pintinhos machos de marca comercial, alimentados com dietas à base de milho e farelo de soja. Foi utilizado delineamento em blocos ao acaso com cinco repetições e 26 aves por unidade experimental. Os tratamentos consistiram na suplementação da dieta basal com NH4Cl a fim de se obter cinco níveis -50; 0; 50; 100 e 150mEq/kg de balanço eletrolítico (BE). O nível de BE influenciou os teores de fósforo, potássio, sódio, PC e PNC, relação Ca:P e a resistência à quebra. A redução do balanço eletrolítico da dieta em nível inferior a 150mEq/kg influenciará negativamente a mineralização e a resistência óssea. A resistência à quebra do tibiotarso não está correlacionada com as concentrações dos minerais de forma individual, mas correlaciona-se negativamente com as concentrações de proteínas colagenosas e não colagenosas.

This study was carried out in order to evaluate the bone chemical composition and breaking force resistance of tibiotarsus birds at 21 days of age. The bone percentage of colagenous proteins (CP), non colagenous proteins (NCP) and minerals (calcium, phosphorus, potassium and sodium) was analyzed. A total of 650 commercial male broiler chicks were fed corn and soybean diets. A completely randomized block design with five replications of 26 birds per experimental unit was used. The treatments consisted of the basal ration supplemented with NH4Cl in order to obtain five levels (-50; 0; 50; 100 and 150mEq/kg) of electrolyte balance. The EB level affected the percentages of phosphorus, potassium and sodium, PC and PNC, Ca: P relation and breaking force resistance. The reduction of EB diets at levels below 150mEq/kg will affect negatively the mineralization and bone resistance. The breaking force of tibiotarsus is not correlated with the mineral concentration individually, but correlates negatively with the concentration of collagenous and non-collagenous proteins.

Expression and ligand binding of bombesin receptors in pulmonary and intestinal carcinoids.

INTRODUCTION: Carcinoids are mainly found in the gastrointestinal (65%) and bronchopulmonary tract (25%). These neuroendocrine tumors secrete a wide range of bioactive peptides, including gastrin releasing peptide and neuromedin B, the mammalian analogs of bombesin. The purpose of this study was to investigate the quantity and localization of bombesin receptors in gastrointestinal and pulmonary carcinoids, and to reveal whether bombesin-like peptides (BLP) and their receptors are of any value in distinguishing pulmonary carcinoids from carcinoids of intestinal origin. METHODS: Carcinoid tumors with pulmonary (no.=9) or intestinal (no.=15) localizations were analyzed by immunohistochemistry, autoradiography, and radioimmunoassay, to examine the presence of bombesin receptor subtypes and determine BLP levels in these tumors. RESULTS: All 3 bombesin receptor subtypes (GRPR, NMBR, and BRS-3) were present on pulmonary and intestinal carcinoids by immunohistochemistry. In pulmonary carcinoids, low receptor ligand binding densities together with high and low BLP levels were found. Intestinal carcinoids showed predominantly high receptor ligand binding densities in combination with low BLP levels. CONCLUSIONS: The expression of bombesin receptor subtypes is independent from the carcinoid tumor origin, and is therefore not recommended as a distinction marker, although carcinoids of pulmonary and intestinal origin possess different receptor binding affinities for bombesin and dissimilar BLP levels. The combined presence of bombesin and its receptors might suggest the presence of a paracrine or autocrine growth loop in carcinoids.

Substance P receptor expression in patients with inflammatory bowel disease. Determination by three different techniques, i.e., storage phosphor autoradiography, RT-PCR and immunohistochemistry.

Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation accompanied by changes in motility. It is known that regulatory peptides like substance P (SP) are important pro-inflammatory peptides which are also involved in neuronal conduction. To get clues for new diagnostic and therapeutic approaches we describe the SP receptor (NK-1) distribution in IBD compared to control intestinal tissue, on mRNA and protein level by three complementary techniques. Autoradiography showed differences within the intestinal wall of control patients; mucosal binding was 17 fmol/g and muscular binding was significantly (p=0.01) higher (98 fmol/g). In inflamed specimens of patients with IBD mucosal SP binding was increased compared to controls (55+/-10 vs 18+/-4 fmol/g mucosa, p=0.002). However RT-PCR showed that the mRNA content of the NK-1 receptor in these samples was not increased. In non-inflamed samples of patients with Crohn's disease (CD) and ulcerative colitis (UC) SP binding was similar as in controls, while mRNA was significantly decreased in CD patients (0.7+/-0.02 vs 4.4+/-0.7, p=0.01) but not in UC patients (4.4+/-0.7 vs 4.1+/-1.4). Immunohistochemistry identified a broad spectrum of NK-1 receptor locations in control intestine. No aberrant expression in IBD was found. This study showed that although there was no difference in location of the SP receptors in IBD patients versus controls, the quantity of SP binding was significantly increased in the inflamed mucosa of IBD patients, while the mRNA level was not increased. Further a difference in mRNA level between non-inflamed tissue of CD and UC patients was shown, with mRNA in CD being lower. These changes in SP receptor expression during chronic inflammation suggest that SP receptors are a potential target for therapeutic regulation of the inflammatory response.

Gastrin releasing peptide receptor expression is decreased in patients with Crohn's disease but not in ulcerative colitis.

BACKGROUND: Gastrin releasing peptide (GRP) and neuromedin B are bombesin (BN)-like peptides involved in regulating motility and inflammation in the gastrointestinal tract, which may be useful in treating inflammatory bowel disease (IBD). Three bombesin-like peptide receptors have been reported, but no studies have investigated their localisation in normal and inflamed human intestine. AIM: To localise and characterise BN receptors in normal intestine and to see whether this is modified in IBD. METHODS: Full thickness intestinal tissue samples were collected from 13 patients with Crohn's disease (CD), 11 with ulcerative colitis (UC), and 19 controls. BN receptor expression was characterised and quantified with storage phosphor autoradiography using BN, GRP, neuromedin B, and the synthetic analogue BN(6-14) as ligands. RESULTS: Only BN receptor type 2 (high affinity for GRP) was present in intestinal tissue. Minimal BN binding was detected in the mucosa. In normal colonic smooth muscle, mean BN binding was 336 fmol/g tissue in longitudinal muscle, including the myenteric plexus, and 71 fmol/g in circular muscle. In CD, colonic smooth muscle BN binding was significantly decreased (longitudinal muscle, 106; circular muscle, 19 fmol/g), in contrast to UC (377 and 62 fmol/g, respectively). In CD, a small (not significant) decrease was seen in ileal muscle compared with controls (111 v 169 and 18 v 32 fmol/g tissue for longitudinal and circular muscle, respectively). CONCLUSIONS: Only the GRP receptor is expressed in human intestine; expression is highest in longitudinal muscle and myenteric plexus of the colon. Expression is decreased in inflamed and non-inflamed colon of CD, but not in UC.

Cocaine withdrawal symptoms and initial urine toxicology results predict treatment attrition in outpatient cocaine dependence treatment.

This study evaluated the ability of cocaine withdrawal symptoms, measured by the Cocaine Selective Severity Assessment (CSSA) and initial urine toxicology results, to predict treatment attrition among 128 cocaine dependent veterans participating in a 4-week day hospital treatment program. The CSSA was administered and a urine toxicology screen was obtained at intake and at the start of the day hospital (about 1 week later). The combination of a positive urine toxicology screen and a high CSSA score at intake predicted failure to complete treatment. Urine toxicology results at the start of the day hospital, but not at intake, predicted failure to complete treatment. Among participants without other psychiatric illness, high CSSA scores at intake predicted failure to complete treatment. The presence of cocaine withdrawal symptoms and a positive urine toxicology screen are clinically useful predictors of treatment attrition.

Medium chain triglycerides activate distal but not proximal gut hormones.

BACKGROUND AND AIMS: Compared to long chain triglycerides (LCT), medium chain triglycerides (MCT) are considered an attractive caloric source in malabsorptive diseases because of their favorable physico-chemical characteristics. The use of MCTis, however, limited by the occurrence of gastrointestinal symptoms such as diarrhoea. We have, therefore, investigated the effects of MCT and LCT on proximal (cholecystokinin; CCK) and distal (peptide YY; PYY) gut hormone secretion. METHODS: Eight healthy volunteers participated in four experiments performed in random order during continuous intraduodenal administration for 360 min of a) saline (control); b) LCT15 mmol/h; c) MCT15mmol/h (equimolar); d) MCT 30 mmol/h (equicaloric). Plasma CCK and PYY were determined at regular intervals (radioimmunoassay). Duodenocecal transit (DCTT) was measured by lactulose H(2)breath test. RESULTS: DCTT during LCT (105 +/- 11 min) was not significantly different from saline (111 +/- 10 min). Both low dose MCT (54 +/- 5 min) and high dose MCT (61 +/- 6 min) significantly accelerated DCTT (P< 0.05). Plasma CCK increased significantly (P< 0.05) during LCT but not during MCT or saline. PYY increased significantly (P< 0.05) not only during LCT, but also during low and high dose MCT but not during saline. CONCLUSIONS: Intraduodenal MCTs a) accelerate intestinal transit; b) do not stimulate CCK release; c) but stimulate release of the distal gut hormone PYY. These results suggest that MCTs are not rapidly absorbed in the proximal gut but probably reach the ileocolonic region and stimulate PYY release.

Effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion in humans.

This study was undertaken to investigate the effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion. Seven healthy subjects participated in two experiments performed in random order during normoglycemia and hyperglycemic clamping at 15 mM. Duodenal outputs of bilirubin, trypsin, amylase, and bicarbonate were measured by aspiration with a recovery marker under basal conditions for 60 min and during continuous infusion of bombesin (1 ng/kg x min) for 60 min. Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were determined at regular intervals. Compared to normoglycemia, during hyperglycemia basal outputs of bilirubin (17 +/- 3 vs. 0.9 +/- 0.4 micromol/60 min), trypsin (24 +/- 4 vs. 4 +/- 1 U/60 min), amylase (12 +/- 1 vs. 3 +/- 1 kU/60 min), and bicarbonate (2.9 +/- 0.5 vs. 1.2 +/- 0.2 mmol/60 min) were significantly p < 0.05) reduced. Bombesin significantly (p < 0.05) increased pancreaticobiliary output during both normo- and hyperglycemia. During hyperglycemia bombesin-stimulated 60-min outputs of bilirubin, trypsin, amylase, and bicarbonate were not significantly different compared to those during normoglycemia. Basal and bombesin-stimulated plasma PP concentrations were significantly (p < 0.05) reduced during hyperglycemia, but plasma CCK levels were not significantly different. It is concluded that acute hyperglycemia reduces basal but does not affect bombesin-induced pancreaticobiliary secretion.

Effect of hyperglycemia on gastric acid secretion during the gastric phase of digestion.

We have examined the effect of an acute stable hyperglycemia on gastric acid secretion during the gastric phase of digestion. Gastric acid output was measured with a recovery marker (phenol red) under basal conditions and after repeated intragastric instillation of a liquid meal in seven healthy subjects on two separate occasions: during normoglycemia (serum glucose, 15 mM). Premeal gastric acid output was significantly (P < 0.05) reduced during hyperglycemia compared with during normoglycemia (2.6 +/- 1.0 vs. 5.8 +/- 1.8 mmol/h). Intragastric meal-stimulated incremental acid output during hyperglycemia was significantly (P < 0.05) reduced compared with during normoglycemia (19 +/- 4 vs. 38 +/- 9 mmol/120 min). Meal-stimulated gastrin release during hyperglycemia was significantly (P < 0.05) reduced compared with that during normoglycemia (4.9 +/- 1.3 vs. 6.6 +/- 1.6 micrograms.1(-1).120 min-1). The intragastric meal induced significant (P < 0.05) increases in pancreatic polypeptide concentrations only during normoglycemia. During hyperglycemia, recovery rates of gastric contents were significantly (P < 0.05) increased compared with during normoglycemia, both before (81 +/- 4 vs. 71 +/- 6%) and after (72 +/- 4 vs. 57 +/- 4%) meal ingestion, pointing to delayed gastric emptying of liquids during hyperglycemia. In conclusion, 1) gastric acid secretion under unstimulated conditions and during the gastric phase of digestion is reduced during hyperglycemia; 2) meal-stimulated gastrin release is significantly reduced during hyperglycemia; 3) the reduction in meal-stimulated acid output is correlated with the reduction in gastrin releases; and 4) pancreatic polypeptide secretion is significantly reduced during hyperglycemia, pointing to impaired vagal cholinergic tone.

Effect of acute hyperglycaemia on basal and fat-induced exocrine pancreatic secretion in humans.

1. We have investigated the effect of acute hyperglycaemia on pancreatico-biliary secretion in healthy subjects. Duodenal outputs of trypsin, lipase, amylase, bicarbonate and bilirubin were measured for 90 min under basal conditions and for 90 min in response to intrajejunal fat administration (1 g/h) on 2 separate days: during normoglycaemia (blood glucose 5 mmol/l) and during acute hyperglycaemia aimed at 15 mmol/l. Plasma cholecystokinin levels, as the major hormonal stimulus of pancreatic and biliary secretion, and plasma pancreatic polypeptide levels, as an indirect measure of vagal-cholinergic tone, were determined at regular intervals. 2. In the basal period pancreatico-biliary secretion was significantly (P < 0.05) reduced during hyperglycaemia compared with normoglycaemia. During normoglycaemia and hyperglycaemia intrajejunal fat significantly (P < 0.05) stimulated pancreaticobiliary secretion. However, during hyperglycaemia, fat-stimulated 90 min pancreatico-biliary secretion was significantly (P < 0.05) reduced compared with normoglycaemia: trypsin (23 +/- 7 units versus 66 +/- 20 units), lipase (36 +/- 8 k-units versus 74 +/- 18 k-units), amylase (8 +/- 2 k-units versus 18 +/- 5 k-units) and bilirubin (32 +/- 8 mumol versus 71 +/- 14 mumol). Plasma cholecystokinin levels increased significantly (P < 0.05) during fat administration and were not different between the two experiments. Plasma pancreatic polypeptide levels were significantly (P < 0.05) reduced during hyperglycaemia both in the basal period and during intrajejunal fat administration. 3. It is concluded that basal and fat-stimulated pancreatico-biliary secretion are significantly reduced during acute hyperglycaemia. Acute hyperglycaemia does not affect intrajejunal fat-stimulated cholecystokinin secretion. Acute hyperglycaemia inhibits basal and stimulated pancreatic polypeptide secretion suggesting vagal-cholinergic inhibition of pancreatico-biliary secretion during hyperglycaemia.

Serum gastrin and mucosal somatostatin in Helicobacter pylori-associated gastritis.

AIMS: The aims were to study gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter infection. METHODS: We measured basal serum gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. RESULTS: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean +/- SEM: 0.80 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 micrograms/g(protein), respectively). We also found significantly lower antral gastritis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16, and 165 +/- 25 micrograms/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. CONCLUSIONS: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.

Effect of hyperglycemia on gastric acid secretion and gastrin release induced by intravenous amino acids.

Intravenous amino acids (IVAAs) are able to stimulate gastric acid secretion. We investigated the effect of concomitant intravenous infusion of glucose, leading to hyperglycemia, on gastric acid secretion induced by IVAAs. Seven healthy volunteers were studied twice, once during normoglycemia and once during acute hyperglycemia with blood glucose concentrations stabilized at approximately 15 mmol/L. Amino acids were infused intravenously at the rate of 10 g/h for 180 min. Acid output was measured by continuous aspiration using a recovery markers. Serum gastrin and plasma pancreatic polypeptide (PP) concentrations were determined at regular intervals. IVAAs significantly stimulated acid output compared with basal values (2.3 +/- 0.2 and 1.4 +/- 0.4 mmol/15 min, respectively, P < 0.05), release of gastrin, and PP during normoglycemia. Hyperglycemia completely inhibited (P < 0.05) IVAA-induced gastric acid output and significantly inhibited (P < 0.05) release of gastrin and PP. We conclude that IVAAs stimulate gastric acid secretion, and gastrin and PP release; acute hyperglycemia reduces IVAA-stimulated acid output, and gastrin and PP release; and circulating nutrients influence gastric acid and gastrointestinal hormone secretion.

Kinetics and morphology of chemically induced popliteal lymph node reactions compared with antigen-, mitogen-, and graft-versus-host-reaction-induced responses.

Changes in the popliteal lymph node (PLN) in mice evoked by a local graft-versus-host (GVH) reaction and by a single injection of various agents into the hind footpad were compared. The drug diphenylhydantoin induced similar weight changes in time as the GVH reaction. More vigorous and protracted reactions were induced by the drug nitrofurantoin and the contact sensitizer dinitrochlorobenzene, whereas the antigens lipopolysaccharide and sheep erythrocytes caused very moderate and short-lasting weight changes. Alterations of lymph node architecture upon injection of diphenylhydantoin resembled those observed during the GVH response. Some quantitative and qualitative differences were noted for nitrofurantoin, but clearly deviant morphological alterations were seen in response to lipopolysaccharide and sheep erythrocytes. The PLN reaction to dinitrochlorobenzene had features of both the GVH reaction and the antigen-induced responses. These findings support the concept that some drugs and chemicals may induce or exacerbate lymphoproliferative disorders by GVH-like mechanisms.