Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both glutamine and glucose are highly utilized by the small intestine in various animal species. They are, however, very partially oxidized, the major known fate of glucose being lactate and alanine, and that of glutamine being citrulline or proline. At variance with the current view that only the liver and kidney are gluconeogenic organs, because both are the only tissues to express the glucose-6 phosphatase gene, this gene is also expressed in the small intestine in rats and humans, and is strongly induced in insulinopenic states, such as fasting and diabetes. Under the latter conditions, the small intestine contributes 20-25% of whole-body endogenous glucose production. The main small intestine gluconeogenic substrate is glutamine and, to a lesser extent, glycerol. Accounting for these fluxes, the phosphoenolpyruvate carboxykinase gene is strongly induced in insulinopenia and, although up to now it had been considered absent from this tissue, the glycerokinase gene is expressed in the small intestine. The production of glucose by the small intestine may be acutely blunted upon insulin infusion. These new data also emphasize the central role of alanine aminotransferase in the coupling of glutamine and glucose metabolisms in the small intestine.
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PMID:New data and concepts on glutamine and glucose metabolism in the gut. 1145 19

The effects of thyroid hormone deficiency in utero on the fetal glucogenic capacity were investigated by measuring glucose production and hepatic levels of glycogen and gluconeogenic enzymes in normal sheep fetuses in the fed and fasted states during late gestation and in those made thyroid hormone deficient by fetal thyroidectomy (TX). In the fed state, fetal TX had no effect on glucose uptake, utilisation or production by the fetus. It also had no apparent effect on the glycogen content or activities of the key gluconeogenic enzymes in the fetal liver. In addition, fetal plasma concentrations of insulin, cortisol, adrenaline or noradrenaline were unaffected by fetal TX in the fed state. In contrast, the rates of fetal O(2) consumption and CO(2) production per kilogram fetal bodyweight were significantly lower in TX than in intact fetuses in the fed state (P<0.05). TX prevented fetal glucose production in response to maternal fasting for 48 h. It also abolished the normal decreases in the fetal glucose carbon oxidation fraction, the rate of CO(2) production from glucose carbon and in the fraction of the umbilical O(2) uptake used for glucose carbon oxidation that occur during fasting in intact fetuses. At the end of the fast, plasma noradrenaline concentrations and hepatic levels of glycogen, glucose 6-phosphatase, fructose diphosphatase and alanine aminotransferase were significantly lower in TX than in intact fetuses. These observations show that thyroid hormones are essential for glucogenesis in the sheep fetus during late gestation and suggest that these hormones act both on the hepatic glucogenic pathways and on the mechanisms activating glucogenesis in utero.
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PMID:Regulation of glucogenesis by thyroid hormones in fetal sheep during late gestation. 1147 42

The goals of the present study were to provide information into the controversy about nitric oxide (NO) status of the liver during endotoxemia and to assess the role of the phosphatase inhibitor cyclosporin A (CsA) during the insult. Rats were injected with saline, lipopolysaccharide (LPS, 10 mg/kg i.p.) or cyclosporin A (CsA, 5 mg/kg. i.p.) + LPS, S-nitroso-N-acetyl penicillamine (SNAP, 0.1 mMikg) + CsA + LPS or molsidomine (molsid, 0.2 mg/kg) + CsA + LPS. Rat hepatocytes were isolated and tested for metabolic competence by the rate of urea synthesis and for lipid peroxidation. Hepatocytes were cultured under various treatments as LPS or cytokine mixture (CM, TNF-alpha 500 U/ml, INF-gamma 100 U/ml, IL-1beta 200 U/ ml) with or without CsA and iNOS expression was evaluated by NO productivity and by RT-PCR. Twenty-four hours after LPS dosing in vivo, the mortality rate was 15%, while CsA pretreatment increased mortality rate to 30% and reduced hepatocyte viability, increased ALT leakage and reduced urea synthesis. SNAP and Molsid resulted in complete survival of rats, increased urea synthesis, increased cell viability and reduced alanine aminotransferase leakage. LPS or CM increased iNOS expression while CsA pretreatment reduced iNOS expression. There was no correlation between lipid peroxide levels in hepatocytes and functional status of hepatocytes under various treatments. This study demonstrates that NO produced during endotoxemia and under the present conditions is protective to the liver and may function as an adaptive mechanism and that the inhibition of iNOS by compounds like CsA produce unfavorable effects.
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PMID:Inhibition of endotoxemia-induced nitric oxide synthase expression by cyclosporin A enhances hepatocyte injury in rats: amelioration by NO donors. 1178 62

The effect of long-term administration of testosterone, progesterone, and a synthetic estrogen, diethylstilbestrol (DES), on intermediary metabolism was studied in a freshwater fish Oreochromis mossambicus. The present study reveals that testosterone, progesterone, and Des specifically control key enzymes involved in carbohydrate, protein and lipid metabolism in the liver of O. mossambicus implying a general influence of sex steroids on intermediary metabolism. The activities of malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH), isocitrate dehydrogenase (ICDH), glucose 6 phosphatase (G-6-Pase), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) are either stimulated or inhibited following the administration of sex steroids. The long-term in vivo i.p. injection of sex steroids intensely reveals that testosterone and progesterone are hyperglycemic, DES is hypoglycemic, testosterone and DES lipogenic, and progesterone antilipogenic (lipolytic) in the present study. It is also established that amino acid catabolism, mostly that of alanine, may be a major source of substrate for gluconeogenesis. A genomic mode of action is proposed for sex steroids for long term treatment, as their action is sensitive to transcription and translation inhibitors.
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PMID:Sex steroids regulate intermediary metabolism in Oreochromis mossambicus. 1248 67

Between August 1992 and May 1997 a total of 56 patients with falciparum malaria and liver disease were seen. The serum bilirubin, mainly of conjugated variety was raised. The ALT was less than 3 times normal with a minimally raised or normal Alkaline Phosphatase (ALP) and prothombin time. The liver function abnormalities were not related to grade of parasitaemia, fever, duration of the illness, nutritional status of the patient or associated medical problems. Treatment of falciparum malaria led to quick reversal of liver function tests.
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PMID:Falciparum hepatopathy: a reversible and transient involvement of liver in falciparum malaria. 1263 72

The present study examined the effect of long-term treatment with cortisol and corticosterone on enzymes of intermediary metabolism, namely malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH), isocitrate dehydrogenase (ICDH), glucose 6 phosphatase (G-6-Pase), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in Oreochromis mossambicus. Cortisol and corticosterone regulate intermediary metabolism in the liver of O. mossambicus as evidenced by changes in the activity pattern of gluconeogenic and lipogenic enzymes and amino-transferases. The long-term in vivo ip administration of glucocorticoids (GCs) suggests hyperglycemic, gluconeogenic, and antilipogenic roles of the hormones in O. mossambicus. The genomic mode of action of GCs is well established in the present study since the long-term treatment is sensitive to the action of transcription and translation inhibitors.
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PMID:Genomic effect of glucocorticoids on enzymes of intermediary metabolism in Oreochromis mossambicus. 1285 99

N-acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic-induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120-140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD50) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6-phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate-pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic-induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.
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PMID:Protective effect of N-acetylcysteine against arsenic-induced depletion in vivo of carbohydrate. 1519 77

The subchronic oral toxicity of microcystin in common carp (Cyprinus carpio L.) was investigated in this study. The fish (mean body weight of 322+/-36 g, n=10) were orally exposed to Microcystis by feeding with bloom scum at a dose of 50 microg microcystins/kg body weight under laboratory conditions for 28 days. Growth assay results showed that microcystin could completely inhibit the growth of carp, but failed to change the fish hepatosomatic index. Ultrastructural examination by electron microscope revealed severe damage in hepatocytes derived from the treated fish. Serum biochemical assays with commercial kits indicated that alanine aminotransferase and aspartate aminotransferase activities were significantly increased as compared to control levels, but gamma-glutamyl transferase, alkaline phosphatase and lactate dehydrogenase activities remained unchanged. Protein phosphatase inhibition assay revealed that the microcystin concentrations were 261.0+/-108.3 ng microcystin-LR equivalent/g fresh weight in hepatopancreas and 38.3+/-12.3 ng microcystin-LR equivalent/g fresh weight in muscle. The latter is above the limit recommended by the World Health Organization for human consumption. Therefore, we recommend that a warning system be instituted for announcing the occurrence of microcystin-producing water bloom and the possible risk of human intoxication.
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PMID:Subchronic oral toxicity of microcystin in common carp (Cyprinus carpio L.) exposed to Microcystis under laboratory conditions. 1553 Sep 63

This study compared the effects of dietary whey protein with dietary casein or soy protein on glycogen storage and glycoregulatory enzyme activities in the liver of sedentary and exercise-trained rats. Male Sprague-Dawley rats (ca. 130 g) were divided into one sedentary and three exercise-trained groups, with eight animals in each group. Casein was provided as the source of dietary protein in the sedentary group while the exercise-trained groups were fed casein, whey, or soy protein. Rats in the exercise-trained groups ran for 30 mins/day, 4 days/week on a motor-driven treadmill. In the exercise-trained rats, animals fed whey protein had higher liver glycogen content than animals in the other two diet groups. Glucokinase activity was significantly higher in rats fed whey protein compared to that in rats fed soy protein, while glucose 6-phosphatase activity was significantly decreased in animals on the whey protein diet compared with those the other two diets. Although 6-phospho-fructokinase activity was significantly lower in the whey protein group than in the soy protein group, we found that fructose 1,6-bisphosphatase activity was significantly higher in the whey group compared with either the casein or soy groups. Pyruvate kinase activity in rats fed the casein diet was significantly higher than in rats fed either the whey or soy protein diets. In addition, hepatic alanine aminotransferase activity and serum alanine level were also increased in the whey protein group compared with the casein or soy protein groups. Taken together, these results demonstrate that the whey protein diet in exercise-trained rats results in significantly higher levels of liver glycogen, because of the combined effects of regulation of rate limiting glycolytic and gluconeogenic enzyme activities and activation of glycogenesis from alanine via alanine amino-transferase.
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PMID:Dietary whey protein modulates liver glycogen level and glycoregulatory enzyme activities in exercise-trained rats. 1561 22

Subchronic exposure to arsenic is associated with alteration of glucose homeostasis. Arsenic treatment (as sodium arsenite) of male Wistar rats (weighing 130-150 g) at a dose of 5.55 mg kg(-1) body weight (equivalent to 35% of LD(50)) (i.p.) per day for a period of 30 days produced hypoglycemia, with associated increased urinary excretion of glucose and depletion of liver glycogen and pyruvic acid contents. Mobilization of free amino acids from kidney to liver was facilitated by arsenic treatment. Arsenic exposure significantly decreased the glutamate-pyruvate transaminase activity in kidney. Glucose 6-phosphatase activity in liver tissue was also significantly decreased after arsenic treatment. In addition to these, liver lactate dehydrogenase activity was elevated due to arsenic treatment. Melatonin supplementation (i.p.) at a dose of 10 mg kg(-1) day(-1) for last five days prior to sacrifice reversed most of the above changes caused by arsenic. Melatonin, being a potent free radical scavenger may reduce arsenic-induced free radical production, and thereby, eliminating its toxic effects. So, arsenic-induced hypoglycemia, with associated glycogenolytic as well as glycolytic activities of liver can be partially counteracted by melatonin supplementation. Accordingly, it may be suggested that melatonin can serve as a prospective protective agent against arsenic-induced metabolic toxicity.
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PMID:Prospective protective role of melatonin against arsenic-induced metabolic toxicity in Wistar rats. 1566 30


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