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

The regulation of heme oxygenase activity in the developing neonate is essential to the control of bilirubin production as well as intracellular heme and hemoprotein metabolism. The coordinated activity of the microsomal enzymes, heme oxygenase and NADPH-cytochrome c (P450) reductase, and the cytosolic enzyme biliverdin reductase is responsible for the degradation of heme. The complete reaction sequence requires oxygen and NADPH, and produces bilirubin and carbon monoxide in equimolar amounts. Although heme oxygenase expresses a rather broad range of substrate affinities, the oxidative degradation of heme is exclusively alpha-specific. Heme oxygenase is found in several tissues, with significant activity levels in the liver, spleen, and erythropoeitic tissue. Heme oxygenase activity is inducible by heme and other metalloporphyrins, hormones, starvation, stress, toxins, and xenobiotics. Heme oxygenase induction is generally considered to be the result of an increased protein synthesis and gene transcription. This hypothesis is supported by recent studies of the heme oxygenase gene that identified inducer element binding sites responsive to metal administration, heat shock, and nutrient availability. In the developing fetus and neonate, hepatic heme oxygenase activity and mRNA levels are elevated above that of the adult. This suggests that the elevated heme catabolism observed in neonates may be associated with an increased transcription of the heme oxygenase gene. The apparent induction of hepatic heme oxygenase during the neonatal period is probably the result of tissue-specific and time-dependent transcriptional regulating factors including potentially hormones and heme. Several metalloporphyrins, such as the tin and zinc porphyrin complexes, inhibit heme oxygenase activity and thus have therapeutic potential for the treatment of neonatal jaundice. Recent studies suggest that the meso- and bis-glycol derivatives of these metalloporphyrins may be more potent inhibitors of heme oxygenase activity in vitro and in vivo than the protoporphyrin structures. As structural analogues of heme, however, these compounds may also have other less desirable effects on the regulation of heme and hemoprotein metabolism, particularly in the developing neonate.
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PMID:Developmental biology of heme oxygenase. 219 31

Specimens of male and brooding female eider (Somateria mollissima) were collected in Svalbard. Chemical analyses revealed hepatic copper concentrations ranging from 20 to 1050 micrograms per g wet weight. This is in agreement with previous results. The selenium, zinc and cadmium values were equal to or slightly higher than previously recorded. It is suggested that the wide variation in copper concentration is a result of differences in intake of copper-containing food among the birds. High selenium intake may enhance copper accumulation. Starvation influences the concentration of zinc and also copper. Zinc concentrations were significantly higher in females. This may be secondary to starvation. The percentage of copper recovered among the soluble proteins was inversely related to the copper content. The distribution of the soluble proteins reflects a normal copper metabolism. Microscopic studies showed prominent dark granules, positive with the rubeanic acid test for copper, confined to hepatocytes. By electron microscopy, the granules appeared as large irregular, electron-dense bodies that, by X-ray microanalysis, were found to contain copper. There were no signs of liver injuries such as necrosis and fibrosis. Apparently, the eider has evolved a high capacity for copper storage.
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PMID:Chemical and morphological studies of liver from eider (Somateria mollissima) in Svalbard with special reference to the distribution of copper. 236 57

Zymomonas mobilis is an unusual microorganism which utilizes both iron-containing alcohol dehydrogenase (ADHII) and zinc-containing alcohol dehydrogenase (ADHI) isoenzymes during fermentative growth. This organism is obligately ethanologenic, and alcohol dehydrogenase activity is essential. The activities of ADHI and ADHII were altered by supplementing growth medium with iron or zinc salts and by iron starvation. Growth under iron-limiting conditions (chelators, minimal medium) reduced ADHII activity but did not prevent the synthesis of the ADHII protein. The inactive form of this enzyme appeared quite stable, was not renatured by iron addition, and persisted in the cell. The iron-induced increase in ADHII activity required de novo synthesis which was blocked by antibiotic additions. The ability of Z. mobilis to synthesize ADHII and ADHI may be advantageous in nature.
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PMID:Modulation of alcohol dehydrogenase isoenzyme levels in Zymomonas mobilis by iron and zinc. 291 64

Circadian variations of zinc and cortisol concentrations in plasma were studied in six healthy adult men. Three of them were tested over two different 24-h periods. Results were analyzed by computerizing a best-fit curve for each 24-h profile. Plasma zinc displayed a morning peak between 8.00 and 9.00 a.m. followed by an almost linear decline throughout the day with lowest values observed shortly before 6.00 p.m. A transitory increase occurred between 6.00 p.m. and 8.00 p.m. followed by a slow decrease reaching its nadir around midnight. Thereafter zinc increased steadily until 8.00 a.m. A similar profile was observed in a seventh subject who was undergoing therapeutic starvation for obesity (fifth day of the starvation period). In all subjects the time course of plasma cortisol fluctuations paralleled that of zinc. Our results confirm the existence of a circadian rhythm in plasma zinc independent of zinc intake and temporally related to the circadian rhythm of cortisol.
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PMID:Circadian variations in plasma zinc and cortisol in man. 298 Aug 24

The nickel transport system of Clostridium thermoaceticum was investigated with 63NiCl2 and an anaerobic microfiltration transport assay. Transport was optimal at pH 7 to pH 7.5 and 65 degrees C and decreased in the presence of metabolic uncouplers and inhibitors. Exogenous nickel was concentrated 3,000-fold over the apparent nickel concentration gradient during typical transport assays. Stored cellular energy appeared to provide a short-term energy source to power nickel transport, and starvation experiments demonstrated external energy source stimulation of nickel translocation. The apparent Km and Vmax for nickel transport by carbon monoxide-dependent chemolithotrophic cells approximated 3.2 microM Ni and 400 pmol of Ni transported per min per mg of cells (dry weight), respectively. Magnesium, calcium, cobalt, iron, manganese, and zinc did not inhibit the transport of nickel.
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PMID:Energy-dependent, high-affinity transport of nickel by the acetogen Clostridium thermoaceticum. 319 12

The essential metal copper, zinc and iron content in starved virgin and pregnant rat tissue has been studied. The copper content of the whole rat, which was actually increased in pregnant rats, decreased in starved pregnant rats. The differences were significant in 19-day pregnant rats. The total copper content of the conceptus was not affected by starvation. Iron distribution and net tissue content showed the same pattern as that of copper. With regard to zinc, however, there was a decrease of its content associated with starvation in rat tissue. This decrease was statistically significant on the 21st day of gestation both in the mother and in fetuses, which marks a difference compared with the copper-iron pattern. It must be pointed out, however, that--with the significant exception of zinc--the maternal stores of the metals are enough to supply the fetus during starvation despite significant reductions in the maternal reserves.
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PMID:Combined pregnancy and starvation effects on rat tissue iron, zinc and copper contents. 334 20

White male growing rats were fed rat chow diet for 4 days after which they were fasted for 72 h. At the end of fasting, rats were allotted into four dietary treatments that varied only in the level of zinc (Zn): Zn-deficient group (ZnD), 30, 90, and 140 ppm of Zn. A group of eight rats were not fasted and were fed the rat chow diet throughout the experimental period. Blood was obtained at intervals from all groups for the measurements of Zn and somatomedin C (SMC) in the plasma. Eight rats were randomly selected at zero time (t0) and at the end of fasting period were killed for the measurement of tibia Zn. At the end of refeeding, all rats were killed for tibia Zn determination as well. Results showed that plasma SMC decreased to the hypopituitary level at the 3rd day of fasting. At 48 and 72 h of refeeding, the levels of plasma SMC increased significantly in all experimental groups and the differences among groups were not significant. The levels of SMC in groups fed 140 and 90 ppm of Zn continued to increase significantly with progressive refeeding. However, in groups fed 30 ppm and ZnD diets the levels of SMC started to decline after 72 h of refeeding. The levels of plasma Zn followed similar trend as SMC levels. In addition, the levels of Zn in the tibia were comparable in all groups with SMC and plasma Zn levels at the end of fasting or refeeding period. Previous reports showed that plasma SMC level is a more reliable index used to monitor nutritional responses; thus, it could be concluded that the level of Zn in the diet should be considered carefully when planning nutritional intervention for severe malnutrition or starvation.
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PMID:Effect of zinc level in the refeeding diet in previously starved rats on plasma somatomedin C levels. 338 59

Serum zinc, measured in obese patients undergoing two weeks of therapeutic starvation (0 kcal, water ad libitum) increased significantly during the starvation period (+48% at day 10) and returned to prestarvation values after refeeding with a 500 kcal diet. Intestinal absorption of zinc was investigated by an oral zinc tolerance test (with 75 mg of zinc acetate) on the second and the tenth day of starvation. No significant differences were observed between the first and the second test. In our experimental conditions 10 days of starvation failed to induce a loss of zinc exceeding 0.75% of the total body stores. It is concluded that the concentration of zinc in blood per se does not regulate intestinal absorption in the absence of a significant change in zinc requirements.
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PMID:The increase in zincaemia provoked by starvation does not influence the intestinal absorption of zinc. 356 20

The effects of starvation and refeeding of 2-wk-old turkey poults on serum and tissue levels of zinc, copper and iron were investigated. Serum concentrations of zinc and copper declined during 4 d of starvation. Refeeding for 24 h following a period of starvation restored serum copper to levels similar to those in the fed controls but failed to elevate zinc levels. Liver concentrations and total quantities of zinc, copper and iron increased throughout starvation. Refeeding the starved poults reduced hepatic metal concentrations but caused a further increase in total metal content. This was apparently related to the large increase in liver mass, and the effect was most pronounced in poults starved 1 d prior to refeeding. Starvation also caused an increased zinc concentration and content and a reduced copper content in the pancreas, duodenal mucosa and kidney. Iron content of the pancreas and kidney increased during starvation, but that of the duodenal mucosa declined. Starvation evoked a progressive increase in the cytosolic zinc concentration from liver, pancreas, duodenal mucosa and kidney. A major part of this increase was accounted for as zinc bound to metallothionein (MT). Refeeding rapidly reduced cytosolic and MT-bound zinc in each of these tissues. It was concluded that starvation and refeeding had major effects on tissue trace metal status. A function is proposed for MT during starvation as a mechanism for the conservation of body zinc stores. Zinc, released as a consequence of tissue catabolism, is repartitioned into a soluble storage site (MT), which can be rapidly mobilized to meet the demands of new tissue synthesis once anabolic metabolism resumes.
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PMID:Effects of starvation and refeeding on tissue zinc, copper and iron in turkey poults. 357 61

1. Measurements were made of the non-oxidative reactions of the pentose phosphate cycle in liver (transketolase, transaldolase, ribulose 5-phosphate epimerase and ribose 5-phosphate isomerase activities) in a variety of hormonal and nutritional conditions. In addition, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities were measured for comparison with the oxidative reactions of the cycle; hexokinase, glucokinase and phosphoglucose isomerase activities were also included. Starvation for 2 days caused significant lowering of activity of all the enzymes of the pentose phosphate cycle based on activity in the whole liver. Re-feeding with a high-carbohydrate diet restored all the enzyme activities to the range of the control values with the exception of that of glucose 6-phosphate dehydrogenase, which showed the well-known ;overshoot' effect. Re-feeding with a high-fat diet also restored the activities of all the enzymes of the pentose phosphate cycle and of hexokinase; glucokinase activity alone remained unchanged. Expressed as units/g. of liver or units/mg. of protein hexokinase, glucose 6-phosphate dehydrogenase, transketolase and pentose phosphate isomerase activities were unchanged by starvation; both 6-phosphogluconate dehydrogenase and ribulose 5-phosphate epimerase activities decreased faster than the liver weight or protein content. 2. Alloxan-diabetes resulted in a decrease of approx. 30-40% in the activities of 6-phosphogluconate dehydrogenase, ribose 5-phosphate isomerase, ribulose 5-phosphate epimerase and transketolase; in contrast with this glucose 6-phosphate dehydrogenase, transaldolase and phosphoglucose isomerase activities were unchanged. Treatment of alloxan-diabetic rats with protamine-zinc-insulin for 3 days caused a very marked increase to above normal levels of activity in all the enzymes of the pentose phosphate pathway except ribulose 5-phosphate epimerase, which was restored to the control value. Hexokinase activity was also raised by this treatment. After 7 days treatment of alloxan-diabetic rats with protamine-zinc-insulin the enzyme activities returned towards the control values. 3. In adrenalectomized rats the two most important changes were the rise in hexokinase activity and the fall in transketolase activity; in addition, ribulose 5-phosphate epimerase activity was also decreased. These effects were reversed by cortisone treatment. In addition, in cortisone-treated adrenalectomized rats glucokinase activity was significantly lower than the control value. 4. In thyroidectomized rats both ribose 5-phosphate isomerase and transketolase activities were decreased; in contrast with this transaldolase activity did not change significantly. Hypophysectomy caused a 50% fall in transketolase activity that was partially reversed by treatment with thyroxine and almost fully reversed by treatment with growth hormone for 8 days. 5. The results are discussed in relation to the hormonal control of the non-oxidative reactions of the pentose phosphate cycle, the marked changes in transketolase activity being particularly outstanding.
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PMID:The pentose phosphate pathway of glucose metabolism. Hormonal and dietary control of the oxidative and non-oxidative reactions of the cycle in liver. 579 34


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