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Page 1 od 905 rezultati
Expanded glutamine repeat enhances complex formation of dentatorubral-pallidoluysian atrophy (DRPLA) protein in human brains.
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The genetic defect in dentatorubral-pallidoluysian atrophy (DRPLA) is expansion of the CAG repeat. The mutant gene is translated into the protein which carries the expanded glutamine repeat. Immunoblots of human brain tissues with and without reduction show that the DRPLA protein is a disulfide-bond
Glutamine synthetase protects against neuronal degeneration in injured retinal tissue.
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The neurotransmitter glutamate is neurotoxic when it is accumulated in a massive amount in the extracellular fluid. Excessive release of glutamate has been shown to be a major cause of neuronal degeneration after central nervous system injury. Under normal conditions, accumulation of synaptically
Glutamine supplementation does not prevent small bowel mucosal atrophy after total parenteral nutrition in the rat.
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Glutamine supplementation to non-lipid parenteral nutrition has been demonstrated to attenuate villus atrophy and increase mucosal DNA content in the rat. This study was performed in order to determine the effects of glutamine supplementation to a balanced TPN mixture (including lipids) on
Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids.
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The aims of this study were to determine whether glutamine infusion prevents the decline in protein synthesis and muscle wasting associated with repeated glucocorticoid treatment. Hormone (cortisol acetate, 100 mg.kg body wt-1.day-1) and vehicle (carboxymethyl cellulose)-treated female rats were
The dipeptide alanyl-glutamine prevents intestinal mucosal atrophy in parenterally fed rats.
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This study was performed to determine whether the addition of alanyl-glutamine (Ala-Gln) can prevent intestinal mucosal atrophy induced by standard solution of total parenteral nutrition (S-TPN). Forty-one male Sprague-Dawley rats weighing 250 g were randomly divided into four groups: group I was
Protective effect of glutamine from glucocorticoid-induced muscle atrophy occurs without alterations in circulating insulin-like growth factor (IGF)-I and IGF-binding protein levels.
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We investigated whether the prevention of glucocorticoid-induced muscle atrophy by glutamine infusion is associated with alterations in serum levels of insulin-like growth factor (IGF)-I and its binding proteins (IGFBPs). Hormone (cortisol acetate [CA], 100 mg/kg body wt/day) and vehicle
Low myo-inositol and high glutamine levels in brain are associated with neuropsychological deterioration after induced hyperammonemia.
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The neuropsychological effect of hyperammonemia is variable. This study tests the hypothesis that the effect of ammonia on the neuropsychological function in patients with cirrhosis is determined by the ability of the brain to buffer ammonia-induced increase in glutamine within the astrocyte by
Alanyl-glutamine prevents muscle atrophy and glutamine synthetase induction by glucocorticoids.
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The aims of this work were to establish whether glutamine infusion via alanyl-glutamine dipeptide provides effective therapy against muscle atrophy from glucorticoids and whether the glucocorticoid induction of glutamine synthetase (GS) is downregulated by dipeptide supplementation. Rats were given
Influence of glutamine and branched chain amino acids on the jejunal atrophy associated with parenteral nutrition.
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Infusions of conventional parenteral nutrients (CPN) are associated with gut atrophy. This may be due to the absence of glutamine in such solutions. Although glutamine is a preferred gut nutrient, it is excluded from CPN because it is unstable at room temperature. This problem may be circumvented
Glutamine prevents pancreatic atrophy and fatty liver during elemental feeding.
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Rats fed an elemental, enteral diet (STD) developed pancreatic atrophy and hepatic steatosis following 60% jejunoileal intestinal resection. An isonitrogenous, isocaloric 2 g/100 ml glutamine-supplemented diet (GLN) significantly attenuated the development of pancreatic atrophy and hepatic steatosis
The influence of parenteral glutamine and branched-chain amino acids on total parenteral nutrition-induced atrophy of the gut.
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We tested the hypothesis that the provision of glutamine and branched-chain amino acids would reverse the gut atrophy that accompanies parenteral nutrition. Three hundred seventy-five rats were randomized into 15 groups to receive either conventional parenteral nutrition, rat food,
Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction.
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This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic
Effect of glutamine-supplemented total parenteral nutrition on recovery of the small intestine after starvation atrophy.
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Intestinal atrophy was induced in rats by infusion of 5% dextrose for 7 days with only oral water allowed. Compared with control animals fed standard rat chow (Purina Mills, St. Louis), the starved animals lost 30.5% of their initial body weight, 34.7% mucosal wet weight, 68.3% mucosal nitrogen
Glutamine dipeptide-supplemented parenteral nutrition reverses gut atrophy, disaccharidase enzyme activity, and absorption in rats.
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BACKGROUND
Total parenteral nutrition (TPN) is associated with intestinal atrophy and dysfunction possibly attributed to the absence of the nonessential amino acid glutamine from commercially available TPN solutions because of the instability of the monoamino acid during heat sterilization and
The effect of glutamine on prevention of glucocorticoid-induced skeletal muscle atrophy is associated with myostatin suppression.
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Excess glucocorticoids (GCs) cause muscle atrophy. Glucocorticoid-induced muscle atrophy is associated with increased intramuscular myostatin expression. Myostatin is a negative regulator of skeletal muscle mass. Glutamine prevents GC-induced muscle atrophy. We hypothesized that glutamine effect on
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