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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of 24-hr starvation on the amino acid pool composition and its concentration ratios with respect to blood and plasma as well as the activities of alanine, aspartate and branched chain amino acid transaminases, glutamate dehydrogenase, glutamine synthetase and adenylate deaminase have been studied in rat brown adipose tissue. Starvation induced a considerable decrease of pool amino acid concentration. Alanine and taurine were the amino acids in which the decrease was more marked. Small changes were observed in the activities of the enzymes studied, with decreases only in glutamate dehydrogenase and adenylate deaminase. These changes agree with a decrease in amino acid utilization in this tissue induced by starvation.
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PMID:Effect of 24-hour starvation on amino acid pool composition and enzyme activities of rat brown adipose tissue. 288 93

The effects of different culture conditions on nitrate reductase activity and nitrate reductase protein from Monoraphidium braunii have been studied, using two different immunological techniques, rocket immunoelectrophoresis and an enzyme-linked immunosorbent assay, to determine nitrate reductase protein. The nitrogen sources ammonium and glutamine repressed nitrate reductase synthesis, while nitrite, alanine, and glutamate acted as derepressors. There was a four- to eightfold increase of nitrate reductase activity and a twofold increase of nitrate reductase protein under conditions of nitrogen starvation versus growth on nitrate. Nitrate reductase synthesis was repressed in darkness. However, when Monoraphidium was grown under heterotrophic conditions with glucose as the carbon and energy source, the synthesis of nitrate reductase was maintained. With ammonium or darkness, changes in nitrate reductase activity correlated fairly well with changes in nitrate reductase protein, indicating that in both cases loss of activity was due to repression and not to inactivation of the enzyme. Experiments using methionine sulfoximine, to inhibit ammonium assimilation, showed that ammonium per se and not a product of its metabolism was the corepressor of the enzyme. The appearance of nitrate reductase activity after transferring the cells to induction media was prevented by cycloheximide and by 6-methylpurine, although in this latter case the effect was observed only in cells preincubated with the inhibitor for 1 h before the induction period.
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PMID:Immunological approach to the regulation of nitrate reductase in Monoraphidium braunii. 291 54

Maternal nutritional deprivation resulted in reduced fetal weight at term gestation (251 +/- 7 vs. 277 +/- 7 g, P less than 0.01) in newborn dogs. Growth-retarded pups developed lower blood glucose levels after 3, 6, and 9 h of neonatal fasting, reduced plasma levels of free fatty acids (FFA) at 9 and 24 h, and lower ketone bodies at 24 h compared with age-matched newborn control pups. Systemic rates of palmitate and alanine turnover were not affected, but systemic glucose turnover was reduced for 3-9 h after birth. The rate of alanine incorporation into glucose from 3 to 9 h was also reduced in growth-retarded pups compared with timed controls. Paradoxically, the rate of incorporation of palmitate into triglycerides was augmented in the smaller growth-retarded pups. Hepatic glycogen content was reduced at every time in the study among growth-retarded pups, whereas the rates of glycogenolysis between birth and 24 h were equivalent in the two pup groups. In contrast, hepatic triglyceride levels were augmented throughout the study in pups with growth retardation. Maternal starvation and lower glucose levels resulted in a lower hepatic energy charge, and augmented cytoplasmic and mitochondrial NAD-to-NADH ratios in intrauterine growth-retarded pups. These data suggest that intrauterine growth retardation in dogs results in fasting neonatal hypoglycemia that is due in part to reduced systemic glucose production. We speculate that reduced rates of gluconeogenesis from alanine and reduced oxidation of alternate fuels such as FFA contribute to hypoglycemia. FFA recycling to triglyceride synthesis rather than oxidative pathways may contribute to the observed reduction of circulating glucose levels.
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PMID:Alterations of fasting glucose and fat metabolism in intrauterine growth-retarded newborn dogs. 292 5

A 5-year-old boy is described who presented with episodes of hypoglycaemia triggered by mild infections or fever. Subnormal glucocorticoid production was confirmed by demonstrating low urinary excretion of free cortisol, low plasma cortisol concentrations that did not rise after glucagon and ACTH stimulation, and by elevated plasma ACTH levels. The selective nature of the abnormality was confirmed by demonstrating normal plasma electrolyte concentrations and blood pressure on a salt-restricted diet. Plasma renin activity and plasma aldosterone levels were also normal and responded appropriately to salt restriction and to frusemide-induced diuresis. Starvation-induced hypoglycaemia was associated with raised levels of blood ketone bodies and low blood alanine concentrations. Catecholamine secretion during hypoglycaemia was reduced. Glucocorticoid replacement therapy was effective in restoring normal glucose homeostasis.
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PMID:Isolated glucocorticoid deficiency: metabolic and endocrine studies in a 5-year-old boy. 298 94

Amino acid transport was studied in C1 cells which contain amplified levels of sodium- and potassium-activated adenosine triphosphatase (Na,K-ATPase), in C4 cells which are ouabain-sensitive revertants, and in parental HeLa S3. Sodium-dependent uptake of aminoisobutyric acid and alanine was increased 2-fold in the amplified C1 cells. After a 6 h amino acid starvation period, the rate of sodium-dependent uptake of methylaminoisobutyric acid was 70-90% greater for C1 than for C4 and HeLa. This uptake was inhibitable by ouabain and the apparent Km values for high affinity uptake were similar in all three lines. Overall, neutral amino acid uptake through Systems A, ASC, and L was 2-fold higher in the Na,K-ATPase amplified C1 cells relative to C4 or HeLa. The induction of System A uptake of methylaminoisobutyric acid after starvation was more rapid in both the amplified C1 cells and the revertant C4 when compared to HeLa, which suggests that the selection for amplification of the Na,K-ATPase produced membrane alterations affecting the adaptive regulation of System A.
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PMID:Alterations in amino acid transport in Na,K-ATPase amplified HeLa cells. 300 Oct 56

Plasma insulin, glucagon, glucose, free fatty acids and glycerol, hepatic cyclic AMP and glycogen, and liver phosphoenolpyruvate carboxykinase (PEPCK), fructose 1,6-bisphosphatase (FBPase), glucose 6-phosphatase (G6Pase) and alanine amino transferase (AAT) activities were examined in adult rats during the first 24 h of either starvation or consumption of a high protein, carbohydrate-free (HP) diet. Under both nutritional conditions, plasma insulin fell within 12 h and remained constant thereafter. Glucagon increased 12 h after the start of the experiment and peaked between 18-24 h. The insulin: glucagon ratio was lower during the last 12 h of the experiment. In both experimental groups, liver cyclic AMP increased progressively and peaked between 15-24 h, but it increase was higher on HP diet than on starvation. Whereas plasma glucose remained low on starvation for 24 h, it returned to normal on consumption of the HP diet. In both groups, liver glycogen fell within 12 h and remained low until the end of experiment. FBPase, G6Pase and AAT did not change on starvation, while they increased toward the end of 1 d HP consumption. During starvation or consumption of the HP diet, PEPCK increased progressively and peaked between 15-24 h, but the increase was greater with the HP diet than with starvation. These findings suggest that in the first 24 hours, the adaptative response of hepatic gluconeogenesis is higher with a HP diet than upon starvation.
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PMID:Comparison between starvation and consumption of a high protein diet: plasma insulin and glucagon and hepatic activities of gluconeogenic enzymes during the first 24 hours. 300 46

The basis for disruption of morphogenesis by depletion of pyridoxine derivatives was studied using a pdxH null mutant of Escherichia coli K-12. Removal of pyridoxal from growing cultures severely inhibited murein synthesis in vivo, whereas simultaneous supplementation with D-alanine effectively prevented inhibition. Extractable alanine racemase was low following such starvation. Selection of mutants overcoming the glycine- or temperature-sensitivity imposed by pyridoxine limitation yielded a variety of phenotypes. The most effective of these extragenic suppressors conferred an elevated alanine racemase activity which was resistant to the effects of pyridoxal removal.
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PMID:Temperature-sensitive murein synthesis in an Escherichia coli pdx mutant and the role of alanine racemase. 306 37

Chicks of king penguin (Aptenodytes patagonica), while only 3-4 months old, tolerate 4-6 months of fasting when they are abandoned by their parents during the subantarctic winter. The body mass of nine chicks, which were followed during this natural winter fast, was 13.1 kg at capture and 3.4 kg after 150 days of fasting, a 74% decrease. The longer phase II (129 days) was marked by lipid mobilization and protein sparing, as indicated by a continuous increase in plasma levels of free fatty acids, glycerol, and beta-hydroxybutyrate, whereas plasma alanine, uric acid, and urea remained stable at low values. In phase III, by contrast, plasma concentrations of lipid-derived metabolites decreased, while plasma alanine, uric acid, and urea increased markedly, indicating an increase in protein utilization. Plasma insulin concentration did not significantly change during either phase II or phase III. Plasma glucagon remained constant during phase II and at the beginning of phase III but increased 2.6 times afterward. Plasma corticosterone increased only slightly during the first 4 months of the fast but reached very high values at the end of phase II and the beginning of phase III (4.7 times basal values); moreover, it further increased 3.1 times before phase III was stopped. Altogether, these data accord with the idea that the outstanding resistance of king penguin chicks to starvation is due to the ability to extensively prolong the situation of protein sparing, which seems to require the maintenance of low plasma concentrations of corticosterone and insulin for up to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma hormone levels in relation to lipid and protein metabolism during prolonged fasting in king penguin chicks. 306 Mar 95

When amino acids that are generally transported through the A system are added to derepressed cultures of CHO-K1 cells or to cultures that are undergoing starvation-derepression, as in the co-repressor (co-r), co-inactivator (co-i), (co-ri) assay, the A system undergoes trans-inhibition, inactivation, and repression. The effect of inactivation and repression is not related to the ability of amino acids to bind to the A system transporter but supports a model in which these amino acids act as co-r's/co-i's, and by binding to a aporepressor/inactivator (apo-ri), the product of gene R1, convert it into a repressor/inactivator (ri). For example, beta-alanine acts as a strong co-r but does not inhibit proline transport through the A system. Hydroxyproline and histidine, although poor inhibitors of proline transport, are very effective as co-ri's. Diaminobutyrate, phenylalanine, alpha-keto-glutarate, pyro-glutamate, isoleucine, and valine, compounds that inhibit A system transport, listed in decreasing order of effectiveness, are all equally poor as co-ri's. Also the Km for the transport of 2-(methylamino)isobutyric acid (MeAIB) through the A system is two times the concentration of MeAIB required to produce one-half inactivation. Amino acid effectors and mutation can modify the conversion of the apo-ri to repressor (r) and inactivator (i). The apo-ri is converted by alanine, serine, proline, and MeAIB to ri, by beta-alanine and tryptophane to r, and by hydroxyproline to r and reduced i. The full constitutive and partial constitutive mutants alar4 and alar2, respectively, are in the same complementation group. Alar4 has no active apo-ri while the rate of derepression of alar2 is twice and the inactivation rate is equal to that of the parent culture.
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PMID:Regulation of the A system of amino acid transport in Chinese hamster ovary cells, CHO-K1: the difference in specificity between the apo-repressor inactivator (apo-ri) and the transporter and the characterization of the proposed apo-ri. 308 25

1. The effect of starvation on the metabolism of gut glutamine and ketone-bodies of peak lactating, non-lactating and virgin rats was investigated. 2. The arterial blood ketone-body concentration was increased by approximately 7-, 6- and 13-fold in 48 h-starved virgin, non-lactating and lactating rats, respectively. 3. The arterial blood glutamine concentration was decreased by approximately 32% in 48 h-starved lactating rats (p less than 0.001). 4. The maximal activity of phosphate-dependent glutaminase was increased or decreased in the small intestine of fed or 48 h-starved peak-lactating rats, respectively. 5. Portal drained viscera blood flow increased by approximately 25% in peak-lactating rats. 6. Arteriovenous difference measurements for ketone-bodies across the gut of 48 h-starved rats showed an increase in net uptake of ketone-bodies by approximately 10-, 17- and 29-fold in virgin, non-lactating and lactating rats, respectively. 7. Glutamine was extracted by the gut of peak-lactating rats at a rate of 487 nmol/100 g of body wt. which was greater by approximately 33% (p less than 0.001) than that of virgin or non-lactating animals. In peak lactating rats, 48 h-starvation resulted in marked decreases in the rates of glutamine removal from the circulation (p less than 0.001) which was accompanied by decreased rates of release of glutamate, alanine and ammonia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glutamine and ketone-body metabolism in the small intestine of starved peak-lactating rats. 313 91


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