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

Amino acid starvation causes an adaptive increase in the initial rate of transport of selected neutral amino acids in an established line of rat hepatoma cells in tissue culture. After a lag of 30 min, the initial rate of transport of alpha-aminoisobutyric acid (AIB) increases to a maximum after 4 to 6 h starvation of 2 to 3 times that seen in control cells. The increased rate of transport is accompanied by an increase in the Vmax and a modest decrease in the Km for this transport system, and is reversed by readdition of amino acids. The enhancement is specific for amino acids transported by the A or alanine-preferring system (AIB, glycine, proline); uptake of amino acids transported by the L or leucine-preferring system (threonine, phenylalanine, tyrosine, leucine) or the Ly+ system for dibasci amino acids (lysine) is decreased under these conditions. Amino acids which compete with AIB for transport also prevent the starvation-induced increase in AIB transport; amino acids which do not compete fail to prevent the enhancement. Paradoxically threonine, phenylalanine, tryptophan, and tyrosine, which do not compete with AIB for transport, block the enhancement of transport upon amino acid starvation. The starvation-induced enhancement of amino acid transport does not appear to be the result of a release from transinhibition. After 30 min of amino acid starvation, AIB transport is either unchanged or slightly decreased even though amino acid pools are already depleted. Furthermore, loading cells with high concentrations of a single amino acid following a period of amino acid starvation fails to prevent the enhancement of AIB transport, whereas incubation of the cells with the single amino acid for the entire duration of amino acid starvation prevents the enhancement; intracellular amino acid pools are similar under both conditions. The enhancement of amino acid transport requires concomitant RNA and protein synthesis, consistent with the view that the adaptive increase reflects an increased amount of a rate-limiting protein involved in the transport process. Dexamethasone, which dramatically inhibits AIB transport in cells incubated in amino acid-containing medium, both blocks the starvation-induced increase in AIB transport, and causes a time-dependent decrease in transport velocity in cells whose transport has previously been enhanced by starvation.
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PMID:Derepression of amino acid transport by amino acid starvation in rat hepatoma cells. 1 7

We have studied the presence of the messenger RNA (mRNA) for the cytosolic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), in rat lung by Northern blot hybridization to a complementary DNA (cDNA) probe. Lung from normal rats contained substantial amounts of this mRNA, although its relative concentration was approximately six times lower than in liver. Fasting produced an eightfold increase in the content of the enzyme mRNA in lung, which could be reverted to normal values by glucose refeeding. Induced diabetes also resulted in a sevenfold increase of the levels of PEPCK mRNA in lung. Dexamethasone, thyroid hormone, dibutyryl cyclic adenosine monophosphate (cAMP), histamine, and serotonin also induced important accumulations of the enzyme mRNA without affecting the concentration of beta-tubulin mRNA measured as reference. Thus, the PEPCK gene appears to be regulated in a similar manner in lung and liver. The results suggest that PEPCK may be involved in lung metabolism in starvation, diabetes, and other specific hormonal situations.
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PMID:Detection and hormonal regulation of the mRNA for cytosolic phosphoenolpyruvate carboxykinase in rat lung. 162

Dexamethasone (DEX) inhibits growth and induces differentiation in rat pancreatic acinar AR42J cells. We wished to determine whether growth and differentiation are mutually exclusive in AR42J cells and whether DEX effects on growth and differentiation are mutually dependent or independent. Inhibition of DNA synthesis, assessed by [3H]thymidine incorporation, was detectable after 6 h, half-maximal after 12 h, and complete after 18-h DEX treatment, at which time incorporation was reduced to 9.0% of control. The half-maximal effective dose for inhibition of DNA synthesis was 0.5 nM, and maximal inhibition was achieved with 10 nM DEX. This dose-response was similar to that previously reported for DEX-induced parameters of differentiation. The rank order of potency for inhibition of DNA synthesis by various steroid hormones was DEX greater than corticosterone greater than aldosterone greater than progesterone. Hydroxyurea or serum starvation inhibited growth to the same extent as DEX but did not induce differentiation. Moreover, hydroxyurea or serum starvation did not block the ability of DEX to induce differentiation. Addition of either EGF or insulin significantly reversed the growth inhibitory effects of submaximal (1 nM) DEX. In cultures released from growth inhibition, 1 nM DEX increased cellular amylase content 5.9- to 6.5-fold, similar to the amylase increase in growth-inhibited cultures. Therefore, growth inhibition and differentiation are independent delayed events regulated by DEX in AR42J cells.
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PMID:Growth and differentiation of pancreatic acinar cells: independent effects of glucocorticoids on AR42J cells. 171 23

In the present study glucose kinetic parameters like pool size, distribution volume and rates of total entry and irreversible loss were determined in four castrated male African pygmy goats during hyperglycemia induced by an intravenous glucocorticoid injection (0.25 mg dexamethasone = DXM per kg body weight). Experiments were done at two different metabolic states, "fed" once daily and "fasted" after three days of starvation. The use of [U-14C]- together with [2-3H]- or [6-3H]-glucose made it possible to show changes in rates of gluconeogenesis, phosphorylation and specific recycling of glucose-C (e.g. lactate/alanine). During glucocorticoid induced hyperglycemia (+45%) in fed animals de novo synthesis of glucose (+5%) and lactate/alanine recycling increased (+4%). Rates of irreversible loss for all applied tracers in fasted animals formed only two thirds of the values of fed animals. During hyperglycemia (+40%) after DXM-injection de novo synthesis of glucose (+8%) and lactate/alanine recycling also increased (+27%). Furthermore the rate of phosphorylation of glucose decreased in fasted pygmy goats. The increase in availability of glucose both in fed and fasted animals is due to an increase in gluconeogenesis. In fasted animals additionally a decrease in the rate of phosphorylation and therefore of the peripheral glucose turnover has to be considered.
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PMID:[The effect of glucocorticoids on glucose metabolism in pygmy goats. 2. Glucose turnover and recycling]. 212 56

Uptake of 3-O-methyl-D-glucoside (3-OMG) into thymocytes was studied to ascertain if it is modulated by endofacial hexokinase activity or by intracellular glucose. (1) The Vmax for net uptake of 3-OMG into rat thymocytes is increased by phorbol 12-myristate 13-acetate (PMA; 40 nM) or starvation for 4 h, and decreased by dexamethasone (1 microM). Starvation for 4 h abolishes the PMA-dependent increase in 3-OMG uptake; this effect is prevented by incubation in 2-deoxyglucose (2-dGlc; 1 mM). (2) Dexamethasone decreases 2-dGlc uptake, increases the rate of 2-dGlc exit and decreases accumulation of free 2-dGlc, consistent with decreased endofacial hexokinase activity. (3) 3-OMG uptake is decreased by preloading the cells with 2-dGlc or glucose, whereas preloading with 3-OMG (40 mM) increases uptake of 3-OMG. (4) The inhibitory effect of preloaded 2-dGlc or glucose on 3-OMG uptake is decreased by PMA. (5) Preloading cells with 3-OMG (40 mM) increases 2-dGlc influx in control and dexamethasone-treated cells, but not into PMA-treated cells. (6) The maximal rate of self-exchange of 3-OMG is similar in control, PMA- or dexamethasone-treated cells. These results are consistent with the following view: 3-OMG uptake is retarded by exchange with cytosolic glucose, or 2-dGlc. PMA, by increasing endofacial hexokinase activity, or starvation depletes glucose from the endofacial surface of the transporter, and hence increase 3-OMG uptake. Dexamethasone, by decreasing endofacial hexokinase activity, increases endofacial binding of glucose, and hence decreases 3-OMG uptake. Cytosolic 3-OMG competes with glucose for endofacial sites, and hence the maximal rates of exchange uptake of 3-OMG are similar in control, PMA- or dexamethasone-treated cells, as the activity of thymocyte glucose transporters is apparently unaltered.
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PMID:Effects of phorbol, dexamethasone and starvation on 3-O-methyl-D-glucose transport by rat thymocytes. Modulation of transport by altered trans effects. 230 67

The effect of hormones on the transcription rate of cytosolic phosphoenolpyruvate carboxykinase and level of mRNA for this enzyme in the rat kidney has been investigated. In renal nuclei isolated from rats given dibutyryladenosine cyclic 3',5'-phosphate (Bt2cAMP) or 8-bromoadenosine cyclic 3',5'-phosphate (8-Br-cAMP), [32P]UMP incorporation into hybridizable phosphoenolpyruvate carboxykinase mRNA increased severalfold within 1 h. Changes in the concentration of cytosolic phosphoenolpyruvate carboxykinase mRNA, measured by hybridization of [32P]cDNA to poly(A)+ mRNA, paralleled alterations in the transcription rate. Dexamethasone treatment of adrenalectomized rats increased the transcription rate and the level of phosphoenolpyruvate carboxykinase mRNA 3-4-fold after 4 h. Both parameters then declined to control values by 8 h. When dexamethasone (5 mg/kg) and Bt2cAMP (25 mg/kg) were given together, the rate of phosphoenolpyruvate carboxykinase RNA synthesis and the level of cytosolic mRNA were not increased more than those with either drug alone. Transcription of the gene for renal phosphoenolpyruvate carboxykinase was not affected by diabetes or glucose refeeding but was increased 2-fold after 24 h of starvation and reduced by bicarbonate feeding after 2 h. We conclude that glucocorticoids and cAMP change the rate of transcription of the phosphoenolpyruvate carboxykinase gene in rat kidney, leading to changes of similar magnitude in mRNA level and, hence, enzyme activity. The results presented here and in previous work [Lamers, W., Hanson, R. W., & Meisner, H. (1982) Proc. Natl. Acad. Sci. U.S.A. 79, 5137] indicate that the transcription rate of the gene for phosphoenolpyruvate carboxykinase in liver and kidney responds to hormones in a tissue-specific manner.
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PMID:Effect of hormones on transcription of the gene for cytosolic phosphoenolpyruvate carboxykinase (GTP) in rat kidney. 298 57

Prenatal starvation causes pulmonary hypoplasia, retarded alveolarization, and reduced surfactant production in newborn guinea pigs. This study examined the potential benefit of simultaneous transplacental dexamethasone, which accelerates fetal lung maturation in other species. Pregnant guinea pigs were placed in 1 of 4 groups: Control (C), fed ad libitum until term (67 days) and given daily saline injections from Day 55 of gestation until term; Dexamethasone (D), fed as Group C but given daily injections of 2.0 mg dexamethasone/kg BW from Day 55 until term; Starved (S), given 50% rations from Day 45 until term and injected as Group C; Starved + Dexamethasone (SD), fed as Group S and injected as Group D. Controls and Group D did not differ in body or lung weight, DNA, protein, or lung volume (VL), but Group D lungs contained more lavageable and tissue surfactant, total alveolar surface area (Sa), and membrane diffusing capacity (DmO2) because of increased alveolar surface density. The S neonates weighed 38% less than controls, with proportional reductions in lung weight, DNA, protein, lavage and tissue phospholipids, VL, Sa septal tissue, capillary surface area (Sc), and DmO2. Compared with these S neonates, the SD neonates did not differ for BW, lung weight, DNA, protein, phospholipids, or VL, but their lungs contained significantly more Sa, Sc, epithelial and endothelial tissue volumes, and a higher alveolar surface density. These differences resulted in an average DmO2 for SD neonates that was indistinguishable from that of controls, and correlated with greater viability among the smallest SD animals compared with those in Group S.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of prenatal starvation and dexamethasone treatment on lung development in newborn guinea pigs. 357 20

The rate of lipogenesis in the liver was increased by glucose injection at birth, mediated by the insulin secretion. In addition, glucagon decreased the rates of lipogenesis and non-saponifiable-lipid synthesis after birth. These rates decreased after prolonged starvation in the newborn rat. Tri-iodothyronine injection increased the rates of lipogenesis enhanced in response to glucose administration after prolonged starvation in liver and brown adipose tissue. Dexamethasone, however, increased the rates of lipogenesis enhanced in response to glucose in liver and prevented the increase in the rates of lipogenesis in brown adipose tissue.
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PMID:Regulation of lipogenesis and of non-saponifiable-lipid synthesis in vivo at birth and after prolonged starvation in the newborn rat. 639 60

Short chain (SCAD), medium chain (MCAD), and long chain acyl-CoA dehydrogenases (LCAD) catalyze the first step of fatty acid oxidation, while isovaleryl-CoA dehydrogenase (IVD) is involved in leucine oxidation. They are homologous flavoproteins belonging to the acyl-CoA dehydrogenase (ACD) family. Electron transfer flavoprotein (ETF) serves as an obligatory electron acceptor for these reactions. We demonstrated that the expression of SCAD, MCAD, and LCAD and the alpha-subunit of ETF (alpha-ETF) showed a similar developmental pattern, while that of IVD was distinctly different from others. The ontogenic pattern of each enzyme in the liver differed distinctly from that in the heart. The degree of glucagon-enhanced ACD expression in vivo and in vitro in both the liver and heart was especially high in fasted rats. Dexamethasone induced all ACD mRNAs in the heart. In contrast, it strongly suppressed mRNAs of all ACDs and alpha-ETF mRNA in the liver, except IVD mRNA. Dexamethasone induced IVD mRNA in both the liver and heart. Starvation strongly stimulated expression of all five genes in various tissues, with the highest in the heart, except the IVD gene which was down-regulated. The degree of induction by 3-day starvation differed in different age groups of rats. Feeding the rats a fat-free diet for 7 days caused a marked increase of IVD mRNA in the heart, whereas the high fat diet for the same period resulted in a severe decrease of the same degree, suggesting a protein-sparing mechanism. However, these manipulations of dietary fat content had little effect on the expression of other ACD genes.
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PMID:Developmental, nutritional, and hormonal regulation of tissue-specific expression of the genes encoding various acyl-CoA dehydrogenases and alpha-subunit of electron transfer flavoprotein in rat. 822 58

Hormonal regulation of a major 20 kDa protein of hamster exorbital lacrimal gland (LG) was studied by SDS-PAGE profile analysis and the purified protein's antisera was used to screen tissues of hamster and other species for crossreacting proteins. This protein was seen in female LG but not in males and late-pregnant or hCG-treated females. Low estrogen state in females after gonadectomy, prolonged light-deprivation, prolonged starvation or lactation increased its level several folds to approximately 20% of LG soluble proteins and similar levels were induced in males after gonadectomy (low androgen state). However, light-deprivation or melatonin treatment-induced low androgen state in males had no effect. In gonadectomized hamsters, this LG protein was obliterated on treatment with androgens, estrogens or thyroid hormones. Only estrogen inhibition of LG 20 kDa was prevented by simultaneous tamoxifen administration. Simultaneous treatment of gonadectomized hamsters with gonadotrophins and estrogen/androgen did not prevent the LG 20 kDa protein's inhibition. Relative potencies of estrogens (3.6 microg daily dose) were: estradiol-17beta approximately diethylstilbestrol > estrone > estradiol-17alpha, while estriol and chlorotrianisene had no effect. Dexamethasone, progesterone, prolactin, hypothyroid state or adrenalectomy had no effect on LG 20 kDa expression. Western blot studies confirmed the marked repression of LG 20 kDa by estrogen androgen and thyroid hormone and detected the protein in tears of females and gonadectomized hamsters but not in males. Interestingly, among other tissues tested, crossreaction was only seen with the estrogen-repressed 24 and 20.5 kDa major male-specific secretory proteins of hamster submandibular glands (SMG) which were previously reported by us. This strongly indicated that the LG and SMG proteins are products of the same or closely related genes. A possible role for these hamster sex-specific LG and SMG major secretory proteins in olfactory communication is suggested.
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PMID:Hormonal effects on hamster lacrimal gland female-specific major 20 kDa secretory protein and its immunological similarity with submandibular gland major male-specific proteins. 1062 3


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