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

Starved cells of Candida utilis accumulated Zn2+ by two different processes. The first was a rapid, energy- and temperature-independent system that probably represented binding to the cell surface. The cells also possessed an energy-, pH-, and temperature-dependent system that was capable of accumulating much greater quantities of the cation than the binding process. The energy-dependent system was inhibited by KCN, Na2HAsO4, m-chlorophenyl carbonylcyanide hydrazone, N-ethylmaleimide, EDTA and diethylenetriaminepenta-acetic acid. The system was specific inasmuch as Ca2+, Cr3+, Mn2+, Co2+ or Cu2+ did not compete with, inhibit, or enhance the process, Zn2+ uptake was inhibited by Cd2+. The system exhibited saturation kinetics with a half-saturation value of 1.3 muM and a maximum rate of 0.21 (nmol Zn2+) min(-1) (mg dry wt(-1)) at 30 degrees C. Zn2+ uptake required intact membranes since only the binding process was observed in the presence of nystatin, toluene, or sodium dodecyl sulphate. Cells did not exchange recently accumulated toluene, or sodium dodecyl sulphate. Cells did not exchange recently accumulated 65Zn following the addition of a large excess of non-radioactive Zn2+. Similarly, cells pre-loaded with 65Zn did not lose the cation during starvation, and efflux did not occur when glucose and exogenous Zn2+ were supplied after the starvation period. Efflux was only observed after the addition of toluene or nystatin, or when cells were heated to 100 degrees C. Cells fed a large quantity of Zn2+ contained a protein fraction resembling animal cell metallothionein. In batch culture, cells of C. utilis accumulated Zn2+ only during the lag phase and the latter half of the exponential-growth phase.
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PMID:Accumulation and storage of Zn2+ by Candida utilis. 0 25

While age is increasing involutiones specific to age can be proofed at the gastrointestinal tract, which lead to a deceleration but quantitative unchanged adsorption. Wrong nutrition concerning to the take up of fat, carbohydrates, proteins and trace elements can be found in greater age very often. By watching a collective of healthy persons beyond the age of 90 years however it turns out that this group keeps a nearly faultless nutrition. The requirements of lysin, methionin and calcium is a little higher in old age than in younger. By intermitting starvation or addition of antioxidants life can be prolonged in experiments on animals, when this therapy starts already in younger age. Starvation in higher age, however, leads to a shortening of life in experiments on animals.
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PMID:[Nutritional problems in old age (author's transl)]. 1 34

Antler blood flow was studied in a 2 year old male reindeer during the last half of the antler growth period using an electromagnetic flow probe chronically implanted around the superficial temporal artery. Arteriovenous (a-v) differences of calcium were measured on antler blood. The blood flow increased from 60--90 ml/min when the antler was half-grown to 100--120 ml/min when fully developed. Subsequently a reduction was observed towards shedding. Positive a-v plasma calcium differences (on average 0.2 mM) were recorded during the period of active growth. Two bulls maintained positive a-v calcium differences after a 48 hour starvation period, in spite of reduced arterial calcium concentrations. Exercise to near exhaustion caused a 2 degrees C rise in the rectal temperature. Antler blood flow was decreased immediately after exercise and returned to pre-exercise values usually within 5--10 min. Since no overshoot in antler blood flow was recorded during the hyperthermia it is concluded that variations in blood perfusion of the antlers are without importance in the defence against hyperthermia during and after exercise.
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PMID:Blood flow, calcium deposition and heat loss in reindeer antlers. 15 81

Na+ transport across frog skin, measured as short-circuit current (SCC) shows perfect temperature compensation in frogs acclimated to 6 degrees, 12 degrees, and 23 degrees C as SCC values observed at the acclimation temperatures are equal (about 13 muA/cm2). Reacclimation experiments show that this is not a starvation effect. While very little temperature compensation is seen in the activity of Na+, K+-ATPase in epidermal homogenates from frog skins, the activity of Mg2+-ATPase shows inverse compensation at assay temperatures from 4 degrees to 48 degrees C. This ATPase is apparently activated either by Mg2+ or by Ca2+ and it probably controls the passive permeability of epidermal cells. It is suggested that the inverse temperature compensation in the activity of this enzyme is the main mechanism by which the observed perfect temperature compensation of Na+ transport across frog skin occurs.
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PMID:Temperature compensation of sodium transport and ATPase activity in frog skin. 15 98

The activity of Ca2+-dependent ATP pyrophosphohydrolase was found to fluctuate during spherule formation of the acellular slime mold Physarum polycephalum under starving incubation. The enzyme activity increased up to 16-fold at the 3rd day of the starvation, then decreased drastically to less than its original level. Column chromatography of the enzyme preparation suggested that the increase in the activity was due to de novo synthesis of a new isozyme. Cycloheximide inhibited the synthesis. The two isozymes were different in their Ca2+ sensitivity, the new one being less sensitive.
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PMID:Change in ATP-pyrophosphohydrolase activity during spherule formation of Physarum polycephalum. 17 39

Treatment during starvation of D. discoideum amoebae with micromolar amounts of A23187 causes an enhanced aggregation. Cells develop the properties of differentiated, aggregation competent amoebae earlier than untreated populations. Ionophore increases the release of calcium, and prevents the excretion of the phosphodiesterase ihibitor normally released in the media. A23187 suppresses the morphogenetic block of some aggregates mutants, suggesting that the ionophore either activates cAMP synthesis and excretion, or increases the cellular sensitivity to extracellular cAMP signals. This might result from the enhanced mobilisation of intracellular calcium
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PMID:[The effect of an ionophore on the aggregation of Dictyostelium discoideum]. 17 27

Starvation did not cause increase of hormone-sensitive lipase in rat epididymal adipose tissue. Adrenaline did not activate lipase in the fat cells, although it accelerated the release of free fatty acids from the cells. The results suggest that the mechanism of the stimulation of lipolysis by adrenaline is different from that in the cyclic AMP theory. Adrenaline-sensitive fat globules were prepared by hypotonic treatment of fat cells. Lipolysis in the fat globules was stimulated by adrenaline. It was shown that adrenaline-induced lipolysis in the fat globules was not due to activation of lipase but to initiation of a reaction between lipase and triglyceride. It is well known that calcium ions are essential for ACTH-induced lipolysis and that the hormone stimulates calcium uptake into adipose tissue. It was demonstrated that calcium ions accelerated formation of a complex between fat and lipase. The mechanism of the actions of adrenaline and ACTH are discussed on the basis of these results.
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PMID:Mechanism of actions of adrenaline and ACTH in fat mobilization. 17 4

The interaction of glucose, the major physiological regulator of insulin secretion, with the beta-cell involves the recognition of glucose as a signal, the transduction of this recognition into an intracellular event and the coupling of the event to the exocytotic discharge of insulin from secretory granules. The following aspects of this system are discussed: (1) the mechanism of insulin release; (2) the evidence implicating Ca2+ and cyclic AMP as coupling factors; (3) the main characteristics of glucose-stimulated insulin release; (4) gluco-receptor models and the evidence for them; (5) possible mechanisms for transduction of the response to glucose; (6) the extent to which the systems of the secretory response to sugars may also be involved in the control of proinsulin biosynthesis; (7) whether starvation induces specific changes in the glucoreceptor system.
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PMID:The control of insulin release by sugars. 18 Dec 21

The effects of glucose, a series of glucose metabolites, nicotinamide nucleotides, Ca2+ and p-chloromercuribenzenesulphonate on adenylate cyclase activity in homogenates of mouse pancreatic islets were studied. The basal activity of the adenylate cyclase was approx. 6 pmol of cyclic AMP formed/30 min per microng of DNA at 30 degrees C. The enzyme activity was stimulated by some 150% by fluoride. Starvation of the animals for 48h had no effect on either the basal or the fluoride-stimulated activity. The adenylate cyclase activity was increased by 40-50% when 17 mM-glucose, 10 micronM-phosphoenolpyruvate or 10 micronM-pyruvate was added to the assay medium. The effect of glucose was unchanged in the presence of 17 mM-mannoheptulose, and mannoheptulose alone had no effect. The other glycolytic intermediates, and the coenzymes NAD+, NADH and NADPH, at concentrations up to 1 mM were without any detectable effect on the rate of formation of cyclic AMP. The insulin secretagogue p-chloromercuribenzenesulphonate inhibited the adenylate cyclase markedly even at a concentration of 10 micronM. Calculated concentrations of free Ca2+ of 10 micronM and 0.1 mM inhibited adenylate cyclase by 29 and 71% respectively. It is concluded that both glucose itself and phosphoenolpyruvate and/or pyruvate are true activating ligands for islet and adenylate cyclase and that inhibition of the cyclase by Ca2+ may be of physiological significance.
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PMID:Effects of glucose, glucose metabolites and calcium ions on adenylate cyclase activity in homogenates of mouse pancreatic islets. 19 80

The sensitivity to alloxan was investigated by blood and urine glucose determination and light and electron microscopic study of the endocrine pancreas in groups of mice differing from each other with respect to food ingestion and treatment before alloxan administration. Because of differences in occurrence of glucosuria, degree and duration of hyperglycemia, and severity of structural lesions, it was concluded that starvation increases the alloxan sensitivity and that pre-treatment with 1.25-dihydroxycholecalciferol (DHCC) or parathormone (PTH), but not with Ca2+, enhances the alloxan effect. The serum-calcium concentration determined 10 minutes after pre-treatment was significantly increased in the group given Ca2+, but not in the groups injected with DHCC or PTH. Starved mice injected with DHCC or PTH 10 minutes before alloxan administration exhibited a pronounced second hyperglycemia of long duration, and extensive, selective B-cell necrosis. Starvation and increased serum concentration of DHCC and PTH are believed, directly or indirectly, to induce B-cell alterations which increase the alloxan sensitivity.
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PMID:Effects of 1.25-dihydroxycholecalciferol, parathormone and Ca2+ on the pancreatic B-cell sensitivity to alloxan. 33 60


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