Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of acute superior mesenteric artery occlusion in the dog has been achieved in every case by isotope scanning of the abdomen using technetium-labelled red cells or technetium-labelled human serum albumin. The white cell count is also significantly elevated, but the changes in the levels of the enzymes CPK, LDH, AST and serum amylase are not specific for actue mesenteric ischaemia. In the human the presence of a normal gut circulation can be demonstrated by isotope scanning provided that the patient is not severely shocked. The presence of a normal gut circulation as shown on the scintigram conclusively eliminates the possibility of acute main trunk occlusion of the superior mesenteric artery. This should be of help in differentiating acute occulusive mesenteric ischaemia from other causes of the acute abdomen. Abdominal scintiscanning is complementary to angiography, which still remains the most precise means of diagnosing acute mesenteric ischaemia. Although the abdominal scintigram is more limited in its application and is not as accurate as angiography, it is quicker to perform, non-invasive, and entirely safe. Abdominal scintiscanning is an excellent screening test to be used in patients suspected of suffering from acute occlusive mesenteric ischaemia.
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PMID:The early diagnosis of acute occlusive mesenteric ischaemia: experimental results and clinical applications. 28 87

Mice infected with Schistosoma mansoni were highly sensitive to the lethal effects of bacterial lipopolysaccharide (LPS). The hyper-reactive state of LPS coincided with the development around the parasite eggs of multiple granulomas in the liver. Elevated aspartate transaminase levels in blood and severe hypoglycaemia in LPS-challenged animals indicated extensive liver parenchymal cell damage. There was also a complete depletion of glycogen in hepatocytes of these animals. From this work and studies on other hepatitis models, it is suggested that individuals affected with granulomatous disorders may be at risk because of everyday exposure to LPS from the gut.
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PMID:Increased hepatotoxicity of bacterial lipopolysaccharide in mice infected with Schistosoma mansoni. 55 82

1. Rosy barb (Puntius conchonius) were exposed to 181 micrograms/l mercuric chloride for 48 h and the activity of acid and alkaline phosphatases (AcP and AIP), aspartate aminotransferase (AAT), alanine aminotransferase (AIAT), lactic dehydrogenase (LDH), and acetylcholinesterase (AchE) were measured in vivo in several organs. 2. The AcP activity was inhibited in the liver, gills, kidneys, and gut but stimulated in the gonads. With the exception of kidney, the AIP activity showed an increase in all the organs examined. The AAT and AIAT were generally inhibited in different organs. An increase in LDH activity occurred in the cardiac and skeletal muscles while the AchE activity was considerably lowered in the brain, gills, and liver. 3. In vitro exposure to mercury at concentrations ranging between 10(-10) and 10(-4) M, inhibited the AIP, AAT, AIAT, LDH, and AchE activities in the tissues examined. The AcP activity was also depressed in all the tissues except in the testes, in which a marginal increase was noted. 4. The in vivo and in vitro effects of Hg were not of similar quality implying sequestration of toxic cations in the intact animals.
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PMID:Use of the fish enzyme system in monitoring water quality: effects of mercury on tissue enzymes. 198 72

Persistent abnormalities of liver function tests occur in approximately 15% of home parenteral nutrition (HPN) patients and are associated with steatosis, steatohepatitis, and, rarely, fibrosis or cirrhosis. Approximately one-third of patients with gut failure on long-term HPN have low total and free plasma carnitine concentrations, and it has been suggested that a deficiency of L-carnitine may be responsible for the steatosis and steatohepatitis in HPN patients. To determine whether administration of L-carnitine is capable of reversing steatosis in HPN patients, 4 adult women on HPN for a mean of 53 mo (range 21-80 mo) were studied before and after 1 mo of intravenous L-carnitine supplementation (1 g/day). All patients had abnormalities in standard liver function tests and low total and free plasma carnitine values. The mean total and free plasma carnitine concentrations and the mean total hepatic carnitine concentration were reduced before supplementation and rose to normal values after treatment (27.4 +/- 2.3 to 35.5 +/- 3.1 nmol/ml, 19.4 +/- 2.8 to 25.7 +/- 2.5 nmol/ml, and 3.5 +/- 0.65 to 6.5 +/- 1.2 nmol/mg of noncollagen protein, respectively). However, there were no significant changes in mean serum aspartate aminotransferase and alkaline phosphatase levels (65 +/- 21 vs. 54 +/- 12 IU and 429 +/- 220 vs. 472 +/- 224 IU, respectively), plasma free fatty acids, plasma triglycerides, hepatic free fatty acid and triglyceride concentrations, or the grade of hepatic steatosis on light microscopy. These results suggest that carnitine deficiency is not a major cause of steatosis and steatohepatitis in patients receiving HPN.
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PMID:L-carnitine therapy in home parenteral nutrition patients with abnormal liver tests and low plasma carnitine concentrations. 312 32

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

Circulating immune complexes (CIC) were measured in 133 biopsy-proven patients with various liver diseases. The correlation between CIC levels and other laboratory findings was investigated in each disease group, in order to assess if the increased C1q-binding activity found in these patients was related to particular features of the disease. CIC levels were not significantly different in HBsAg-positive and HBsAg-negative patients. No correlation was found between CIC levels and serum bilirubin, AST, ALT and C3 levels. A negative correlation with C4 levels and a positive correlation with immunoglobulin levels were found in the majority of the patients, while prothrombin time and albumin levels were negatively correlated to CIC levels only in patients with chronic active hepatitis. Increased CIC levels could represent a response to gut-associated antigens, a passive accumulation due to reduced hepatic function or both.
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PMID:Significance of circulating C1q-binding activity in chronic liver disease: a study of 133 cases. 633 89

We report that keratin 8 (mK8) gene disruption causes colorectal hyperplasia in FVB/N mice. The intestinal lesions affect uniformly the cecum, colon, and rectum but not the small intestine. The elongation of the crypts is accompanied by an inflammation of the lamina propria and submucosa. Hepatic, renal, and pancreatic functions tested in clinical assays are within nonpathological range, suggesting that the major defect lies in colonic epithelial cells. Still, small but consistent elevation in the hepatic enzymes alanine (AST) and asparate (ALT) aminotransferase are observed, along with a 70% increase in spleen weight. No homozygous mouse line has been established, because of a markedly reduced fertility of the mK8-/- females. Previously, we reported that the mK8- targeted mutation causes embryonic lethality in (C57B1/6x129Sv) mice. This strong effect of the genetic background on the mK8- mutant phenotype emphasizes the importance of using several inbred mouse strains to reveal the polygenic contribution to mutant phenotypes. Our results demonstrate that genetic modifiers of K8/K18 filament functions, with profound effects on embryogenesis and gut functional integrity, are differentially active in the FVB/N and C57B1/6 genetic backgrounds. More importantly, the increase in mK8-/- gut epithelial cell number, rather than cell disruption, contrasts with the known function of epidermal keratins in providing mechanical strength.
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PMID:Colorectal hyperplasia and inflammation in keratin 8-deficient FVB/N mice. 752 56

Liver injury is common in patients following hemorrhage and sepsis. There are multiple etiologies for this liver injury which involve both decreased nutrient blood flow and direct cellular injury. Enteral nutrients vasodilate gut blood vessels and increase blood flow to the intestines and liver. Since enteral nutrients vasodilate gut blood vessels, we wondered whether luminal nutrition would prevent hepatic injury during shock states. We randomized Sprague-Dawley rats to saline or enteral nutrition via duodenal feeding tubes. Animals were then subjected to 60 min of hemorrhagic hypotension or intraperitoneal injection of lipopolysaccharide (LPS). Liver injury was assessed by measuring levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) before and after hemorrhage or LPS. Enteral nutrients significantly decreased liver injury following hemorrhage. AST increased from 246 +/- 17 to 1605 +/- 593 U/L in saline animals and 283 +/- 39 to 551 +/- 94 U/L in enterally fed animals. ALT increased from 60 +/- 4 to 726 +/- 355 U/L in saline animals and 61 +/- 6 to 161 +/- 38 U/L in enterally fed animals. Enteral nutrients did not significantly alter the increase in AST/ALT following LPS. These results indicate that enteral nutrients can decrease liver injury following hemorrhagic hypotension.
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PMID:Enteral feeding minimizes liver injury during hemorrhagic shock. 774 61

Since the amounts of hepatogenous enzymes discharged into the intestinal tract remain unknown, this study was initiated to evaluate the amounts of the enzymes in the intestinal tract. Whole gut lavage fluid (polyethyleneglycol electrolyte solution) was administered orally to 42 subjects, consisting of 5 patients with hepatoma, 10 with chronic hepatitis, 10 with colon polyps, and 17 control subjects without liver disease. Two hr after the large intestinal lavage, the digestive tract juice was aspirated by colonoscopy, and the bilirubin (Bil), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) in the aspirates were measured. A positive correlation between the AST and LDH values was found, and a significant difference in these values between the hepatic disorders and the normal controls was noticed. A significant positive correlation between the ALP and Bil values was found, and a statistical difference in these values between the group of colon polyps and the controls and other groups was observed. This lavage fluid technique enables to estimate the amounts of hepatic enzymes discharged into the intestinal tract, thereby opening a new avenue for future enzyme research.
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PMID:Enzymes in intestinal juice from patients with liver diseases and colon polyps: measurement of bilirubin, alkaline phosphatase, aspartate aminotransferase and lactate dehydrogenase. 872 97

The cDNA encoding the precursor polypeptide for schistostatins, allatostatin-like peptides which have been shown to inhibit peristaltic movements of the lateral oviducts of Schistocerca gregaria, has been cloned and sequenced. Translation of this sequence reveals the presence of a pre-proschistostatin consisting of 283 amino acids. It contains ten different peptide sequences which are flanked by dibasic cleavage sites and C-terminal amidation signals. Eight of these peptides were identical to the schistostatins (or Scg-ASTs) that were previously purified from Schistocerca gregaria brain extracts. Two novel peptide sequences were discovered. One of these is the first AST-like peptide which has a C-terminal valine residue. Two peptides contain within their sequence an internal dibasic site which suggests a possible role for alternative processing and/or degradation. The schistostatin precursor differs from cockroach pre-proallatostatins in size, in sequence and in organization. It contains a lower number of peptides (10 versus 13 or 14) which are interrupted only once by an acidic spacer region (versus four in Diploptera punctata and Periplaneta americana). Northern analysis showed the presence of a 2.4 kb mRNA band in the locust central nervous system and midgut. This indicates that schistostatins, like other ASTs, are a good example of insect brain/gut peptides.
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PMID:Molecular cloning of the precursor cDNA for schistostatins, locust allatostatin-like peptides with myoinhibiting properties. 890 49


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