Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrin-releasing peptide is a 27-amino acid peptide recently isolated from porcine gut. It shares a common C-terminal decapeptide homology with bombesin (except for a His/Gln interchange at residue 8 from C-terminus). Synthetic porcine gastrin-releasing peptide was shown to release gastrin 5 min after intravenous injection in rats. Given intracisternally (0.3--3 microgram), but not intravenously (1--10 micrograms), gastrin-releasing peptide caused a dose-dependent reduction in gastric secretion (volume and acidity) and elevation in plasma gastrin levels measured 2 h after peptide injection and pylorus ligation in rats. Gastrin-releasing peptide given intracisternally had long acting, reversible, and specific inhibitory effects. Gastrin-releasing peptide blocked the secretion of acid evoked by 2-deoxy-D-glucose or TRH given intracisternally or by histamine given subcutaneously. The acetylated C-terminal octapeptide fragment of gastrin-releasing peptide inhibited gastric acid secretion as effectively as gastrin-releasing peptide. Acetylated C-terminal heptapeptide did not. These results demonstrated that gastrin-releasing peptide has the capability to act in the brain to inhibit basal and stimulated gastric secretion and its antisecretory effect does not depend on a decrease in gastrin release. The presence of bombesin immunoactivity in rat brain and its ability to act through the brain to inhibit gastric acid secretion suggest that bombesinlike peptides may be chemical messengers involved in central nervous regulation of gastric secretion.
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PMID:Central nervous system inhibition of gastric secretion in the rat by gastrin-releasing peptide, a mammalian bombesin. 723 37

Fluorescence staining characteristics of "large vacuoles," i.e. vacuoles ranging up to almost cell size, were studied in suckling rats and pigs. In the distal epithelium of the small intestine of suckling rat, yellow autofluorescence and accumulation of orally administered FITC-dextran were observed in the supranuclear vacuole. In both species the weakly basic amino dye acridine orange (AO) stained the nuclei at neutral pH bright yellow-green and the transport and digestive vacuoles bright red or orange. It is concluded that trapping and accumulation of the dye (red shift) were due to the acidity of the vacuolar interior. Assessment of the vacuolar pH in rat enterocytes is in agreement with published data on lysosomal pH values. Acidic buffers, lysosomotropic and destructive agents, or illumination with bright light induced irreversible fading of AO-stained vacuoles; the color of the porcine transport vacuoles was the most labile. This fading was used to differentiate vacuoles from other structures, e.g., vacuolar inclusion bodies and goblet cells. In suckling rat, staining characteristics of the gut epithelium changed on Days 19 and 20 of postnatal age. Detection of acidity in the distal (digestive) vacuoles supports the lysosome-like nature of their function. They appear to constitute an auxiliary, intracellular digestive system for the young animal. However, the function of acidity in the non-digestive transport vacuoles of newborn pig is unclear.
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PMID:Demonstration of acidity in intestinal vacuoles of the suckling rat and pig. 750 41

Enteral nutrition (EN) has several advantages over parenteral nutrition (PN) for postoperative/posttrauma patients. Modern technologies for tube-feeding have made early EN possible. Jejunal tube-feeding has advantages over gastric tube-feeding: faster metabolic recovery, less vomiting, and less risk of regurgitation and aspiration. Immediate or early EN stimulates the splanchnic and hepatic circulations, improves mucosal blood flow, prevents intramucosal acidosis and permeability disturbances, and eliminates the need for stress ulcer prophylaxis. Saliva containing important antimicrobial substances and gastric acidity are important in sepsis prevention. Chewing, saliva, and gastric acidity support gastric nitric oxide (NO) release, important for mucosal blood flow, gastrointestinal (GI) motility, mucus formation, and bacteriostasis. An oral supply of NO-donating substances and chewing of nitrate-rich food, such as lettuce or spinach, can be useful. Oral and mucosa-protective lipids are recommended. H2 blockers and saliva-inhibiting drugs are avoided. Immediate EN should be given, starting with 25 ml/hr and increasing to 100 ml/hr over 24 to 48 hours. For the immunocompromised patient special attention should be given to the purity of water. Bottled water can contain bacteria such as Pseudomonas. Food antioxidants such as glutathione, vitamin E, and beta-carotenes are important. Ingredients for the colonic mucosa are important. Approximately 10% of caloric need is satisfied by so-called colonic food (prebiotics), fermented at the level of the colonic mucosa to produce colonic mucosa nutrients and to prevent gut origin sepsis. More than 10 g of fiber per day is recommended. The fermenting flora (probiotic flora) is deranged owing to disease or antibiotic treatment, and resupply of flora is important. A new concept of ecoimmune nutrition is presented for enteral supply of mucosa-reconditioning ingredients: new surfactants, pseudomucus, fiber, amino acids such as arginine, and mucosa-adhering Lactobacillus plantarum 299.
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PMID:Nutritional support to prevent and treat multiple organ failure. 866 38

Colonization of the gut by intestinal bacteria begins at birth and progresses rapidly in the immediate postnatal period. Host defense mechanisms that mediate enteric colonization include gastric acidity and intestinal motility. The small bowell overgrowth syndrome is a condition characterized by large numbers of bacteria, often anaerobes, in the upper intestine. Steatorrea, carbohydrate malabsorption and abdominal pain are frequently present. Predisposing conditions are localized anatomic disorders (surgical blind loops, small bowel strictures caused by surgery or Crohn's disease, short-gut syndrome without ileocaecal valve), motility derangements or reduction of gastric acidity. Diagnosis of the overgrowth syndrome is often difficult and quantitative cultures of jejunal-aspirated fluid is the best diagnostic test. Antimicrobial therapy directed against anaerobes is often successful, but the best therapeutic approach is the correction of predisposing conditions, if present.
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PMID:[Infected bowel syndrome]. 866 82

Occlusion of feeding tubes is a common and costly complication of enteral feeding. Although the composition of feeding formulas, the size, design, and material of the feeding tube, and the rate of delivery have been considered as factors that determine the rate of tube occlusion, little information is available on the effect of the luminal content of the gut on tube occlusion. Enteral feeding tubes are placed either in the stomach or postpylorically, in the small intestine. The chemical composition of these regions including acidity and bile salt concentration may vary. Since acidity has been shown to promote tube occlusion and bile salts have detergent-like properties, these chemical differences in the luminal environment may be important to tube occlusion. To test the idea that bile salt inhibits acid-promoted occlusion of feeding tubes, in an in vitro study, we compared the time-to-complete occlusion of four groups of formula-filled feeding tubes (six tubes in each group) immersed in an acidic solution (pH 3.0) containing 0 (control), 10, 20, or 40 mM of taurocholate. We found that although 33% of the feeding tubes were occluded within 12 hours in the absence of exposure to bile salt, none were occluded when 20 or 40 mM of taurocholate was added to the acidic solution. After 24 hours, 40 mM of taurocholate inhibited acid-promoted occlusion of 67% of the feeding tubes. Thus 0 to 40 mM of taurocholate still inhibited acid-promoted tube occlusion in a dose-dependent fashion (p < .05). Acidity and the concentration of bile salt may work together, but in opposite directions, as luminal factors that determine the rate of occlusion of feeding tubes.
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PMID:Bile salt inhibits acid-promoting feeding tube occlusion. 880 28

Numerous factors have the potential to affect the amount of forage or pasture eaten by ruminant animals, including gut capacity, ability of tissues to metabolize nutrients, ruminal acidity, and osmolality. Much research into the control of food intake has tested one particular theory, often by applying greater degrees of stimulation than occur naturally, and is then unable to explain how physiological changes in that stimulus can be responsible for controlling intake. We have found that the effects of two or three stimuli (sodium acetate, sodium propionate, ruminal distension) applied together were additive. As to the site of this integration, receptors in the rumen wall are sensitive to both mechanical stimulation and acids, with transmission of impulses in vagal afferent fibers probably modulated by the osmolality of ruminal fluid. Thus, a certain degree of integration ("polymodal") is likely to have occurred at the level of the transceiving organ. A second level of integration is "polytopic." In this level stimulation of one visceral site modifies the effects of the same type of stimulus at another site. A third level of integration occurs in the central nervous system, whereby the effects of visceral stimulation might be balanced with signals from other stimuli (e.g., the special senses) to determine whether feeding should take place at any given moment. The thesis presented is that the central nervous system receives a nonspecific signal from the viscera; the animal might then learn to eat that amount of food that minimizes the competing discomforts of excessive abdominal visceral stimulation and shortage or imbalance of nutrients.
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PMID:Integration of regulatory signals controlling forage intake in ruminants. 899 18

The oral toxicity of gamma-cyclodextrin (gamma-CD) was examined in a 13-week feeding study in which four groups of four male and four female Beagle dogs received gamma-CD in the diet at concentrations of 0 (control), 5, 10, or 20%. No treatment-related changes were noted in behavior or appearance of the dogs and no mortalities occurred. Transient diarrhea occurred in some dogs of the 5 and 10% dose groups and in all dogs of the 20% dose group. However, all dogs remained in good health and gained weight. During the last 6 weeks of the study, the males of the 20% dose group gained less weight, but body weights were not significantly reduced in comparison to controls. Food intakes and food efficiencies were comparable among all groups. No treatment-related differences were observed with respect to ophthalmoscopic examinations, hematological parameters, clinicochemical analyses of the plasma, and semiquantitative urine analyses. Only the urinary pH was slightly below control levels in males of the 20% dose group. No abnormalities were seen at necropsy that could be attributed to treatment. The organ weight data revealed some cecal enlargement in the 10 and 20% dose groups. Relative ovary weights were significantly increased in the 10 and 20% groups but this was probably a result of an unusually low ovary weight in the controls. An increase of relative liver weights in males of the 10 and 20% dose groups also was considered to lack toxicological relevance because it was not associated with changes in plasma liver enzyme levels or histopathological changes. On microscopic examination, no treatment-related effects were observed in any of the various organs and tissues. In conclusion, transient diarrhea, cecal enlargement, and a slightly increased acidity of the urine were the only treatment-related effects reported. These changes are well-known physiological responses to the presence of increased amounts of undigested, fermentable carbohydrates in the lower gut. At the high applied intakes an incomplete digestion of gamma-CD and/or a partial inhibition of pancreatic amylase by gamma-CD could account for these effects. It is concluded that daily gamma-CD consumption of up to 20% in the diet (approximately 7.7 g/kg body wt in male and 8.3 g/kg body wt in female dogs) was tolerated without any toxic effects.
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PMID:Subchronic (13-week) oral toxicity study of gamma-cyclodextrin in dogs. 967 70

A current model for carotenoid transport and absorption in the gut proposes an initial solubilization in the oil phase of dietary emulsions followed by incorporation of the carotenoids in mixed bile salt micelles. To assess the relevance of the first stage of this model to what is observed in vivo we have examined the transfer of carotene from carrot juice to olive oil. Increased acidity enhanced the transfer from both whole juice and carotene crystals isolated from carrot chromoplasts. The transfer was significantly slower from whole juice. By using exogenous beta-carotene and measuring its transfer to oil in the presence and absence of carrot juice we have demonstrated that the inhibition of the transfer in juice arises, at least in part, from soluble juice factors. The inhibition is relieved by a fall in pH, which leads to lowering of the electric potential at the oil/aqueous phase interface and aggregation of carrot tissue including crystalline carotene. Under conditions of low pH, oil droplets adhere to the tissue aggregates, allowing carotene to pass into the oil. Our results provide an explanation for why carotene absorption in vivo is depressed by conditions of low gastric acidity.
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PMID:Low pH enhances the transfer of carotene from carrot juice to olive oil. 983 78

The author studied methicillin-resistant Staphylococcus aureus (MRSA) proliferation in the rat gut which was influenced by gastric acid inhibition and the administration of antibiotics. When male Wistar rats were bred by total parenteral nutrition (TPN), and were continuously administered famotidine 4 mg/kg per day, the gastric acidity was observed to decrease to pH 6.4+/-0.1. However, when they were bred by TPN, and histamine 4 mg/kg per hour was continuously administered, the gastric acidity was observed to increase to pH 1.9+/-0.4. MRSA was thus able to cross over to the small intestine only during the famotidine medication. If rats were intravenously administered latamoxef (LMOX) after an oral inoculation of MRSA, then the viable MRSA counts in the stomach, small intestine, and large intestine all decreased on day 4. In contrast, if the gastric acidity decreased and the rats were treated by an oral administration of kanamycin and metronidazole before an oral inoculation of MRSA and thereafter were administered LMOX, then the MRSA count significantly increased. It is thus concluded that a suppression of gastric acid and a great disorder of the intestinal flora is indispensable for the colonization of MRSA into the small intestine, while in vitro the propagation of MRSA requires a continuity of suppression absent in the bacterial flora.
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PMID:Methicillin-resistant Staphylococcus aureus proliferation in the rat gut is influenced by gastric acid inhibition and the administration of antibiotics. 1021 63

Botulinum neurotoxin (BoNT) is one of the most potent toxins known. BoNT is also a food poison, which means that the toxin must survive the protease action and acidity of the gut. A group of neurotoxin-associated proteins which are only beginning to be identified and characterized are believed to be responsible for this protection. Hn-33 is a 33 kDa polypeptide which is a major component of the type A botulinum neurotoxin complex. Crystals of Hn-33 have been grown by vapour-diffusion techniques. They belong to a primitive orthorhombic space group and diffract to a resolution of 2. 6 A, with unit-cell parameters a = 130.3, b = 122.2, c = 37.2 A.
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PMID:Preliminary crystallographic studies of a protease resistant botulinum neurotoxin associated protein Hn-33. 1032 96


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