Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney and liver mitochondria of rat, rabbit and guinea pig are able to transform 3-hydroxy-3-methylglutarate into acetoacetate, whereas ox liver mitochondria and rat mitochondria of heart, diaphragm and brain do not exhibit such an activity. Starvation and streptozotocin treatment decreases the formation of acetoacetate from 3-hydroxy-3-methylglutarate. Addition of acetoacetate and succinate to the incubation media of mitochondria results in a decrease in the transformation of 3-hydroxy-3-methylglutarate into acetoacetate. A 3-hydroxy-3-methylglutaryl-CoA hydrolase is present in rat liver mitochondria; the activity does not show appreciable changes after starvation or streptozotocin treatment.
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PMID:Formation and utilization of 3-hydroxy-3-methylglutarate in liver mitochondria of starved and streptozotocin-diabetic rats. 9 38

Fusarium graminearum A 3/5 possesses a high affinity system (Km = 32 +/- 8 microM; mean +/- SE) for uptake of choline, which was shown to be energy-dependent and constitutive. The maximum rate of choline uptake by this system was repressed by ammonia and glucose, showing a three-fold increase in maximum activity after nitrogen (2 h) or carbon (4 h) starvation. The system was highly specific for choline with only dimethylethanolamine (Ki = 198 +/- 29 microM), betaine aldehyde (Ki = 95 +/- 14 microM) and chlorocholine (Ki = 352 +/- 40 microM) acting as competitive inhibitors. Hemicholinium-3 acted as a mixed (non-competitive) inhibitor (KIES = 1.9 +/- 0.6 microM; KIE = 3.6 +/- 1.9 microM).
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PMID:Choline transport in Fusarium graminearum A 3/5. 162 23

The fraction of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase in the dephosphorylated (active) form in rat liver in vivo was measured after various experimental treatments of animals. Intraperitoneal injection of glucose (to raise serum insulin concentrations) into rats 4 h into the light phase (L-4) resulted in a transient (30 min) increase in the expressed (E)/total (T) activity ratio of HMG-CoA reductase without any change in total activity (obtained after complete dephosphorylation of the enzyme). Conversely, intravenous injection of guinea-pig anti-insulin serum into rats 4 h into the dark phase (D-4) significantly depressed the E/T ratio within 20 min. Intravenous injection of glucagon into normal rats at this time point did not affect the degree of phosphorylation of the enzyme, in spite of a 10-fold increase in hepatic cyclic AMP concentration induced by the hormone treatment. A 3-fold increase in the concentration of the cyclic nucleotide induced by adrenaline infusion was similarly ineffective in inducing any change in expressed or total activities of hepatic HMG-CoA reductase. However, when insulin secretion was inhibited, either by the induction of streptozotocin-diabetes or by simultaneous infusion of somatostatin, glucagon treatment was able to depress the expressed activity of HMG-CoA reductase (i.e. it increased the phosphorylation of the enzyme). Therefore insulin appears to have a dominant role in the regulation of the phosphorylation state of hepatic HMG-CoA reductase. In apparent corroboration of this suggestion, short-term 4 h food deprivation of animals before D-4 resulted in a marked decrease in the E/T activity ratio of reductase, which was not affected further by an additional 8 h starvation. By contrast, the total activity of the enzyme was not significantly affected by 4 h starvation, but was markedly diminished after 12 or 24 h starvation. Longer-term starvation also produced a chronic increase in the degree of phosphorylation of the enzyme. These results are discussed in relation to the role of reversible phosphorylation in the control of hepatic HMG-CoA reductase activity in vivo.
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PMID:Acute effects of starvation and treatment of rats with anti-insulin serum, glucagon and catecholamines on the state of phosphorylation of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase in vivo. 288 48

Our previous studies suggested that crypt size enlarged and that proliferation rate might be greater in the small intestine of rats during senescence. Crypt cell numbers and crypt cell proliferation rates, using the vincristine-induced metaphase arrest technique, now have been measured in the colon of aging and young Fischer 344 rats. The proximal colon of 26-28-mo-old unfasted rats had 10% more crypt cells and a higher proliferative rate than 3-4-mo-old young controls. In the distal colon, the crypt cell proliferation rate in aging rats was 56% greater than in the young. A 3-day fast reduced crypt cell proliferation about fourfold in young rats but only by 20% in aging rats. One-day refeeding abruptly increased the crypt cell population and proliferation rate in rats of both age groups. The crypt zone of proliferating cells from aging rats was broader than that seen in young rats. In addition, starvation lowered colonic crypt cell cycling rate much less in aging than in young animals. We conclude that the colons of aging rats demonstrate a hyperproliferative state and a failure to adapt appropriately to changes in food intake. These observations may be relevant to states of altered proliferation that occur in the premalignant colon.
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PMID:Colonic proliferation is increased in senescent rats. 318 79

Ribonucleotide reductase in mammalian cells is composed of two nonidentical subunits, proteins M1 and M2. Protein M2 contains a tyrosyl free radical, essential for activity, which can be quantified directly in frozen, packed cells by EPR spectroscopy. A 3-7-fold increase in the concentration of tyrosyl radical-containing M2 subunit was observed when mouse mammary tumor TA 3 cells passed from the G1 to the S phase of the cell cycle. Similar results were obtained with cells synchronized by isoleucine starvation or separated by centrifugal elutriation. Addition of deuterated tyrosine to cells give rise to a different EPR signal in newly synthesized protein M2. Pulse-chase experiments with deuterated tyrosine showed unequivocally that the S phase-correlated increase in radical-containing M2 subunit was due to de novo protein synthesis. Labeled M2 molecules disappeared with a half-life of 3 h, and therefore new molecules must be synthesized at a high rate during the S phase. In contrast, after hydroxyurea inactivation, cells rapidly regenerated the tyrosyl radical in already existing protein M2 molecules. This enzyme activation mechanism is clearly different from the one responsible for regulating protein M2 activity during the cell cycle.
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PMID:Cell cycle-dependent regulation of mammalian ribonucleotide reductase. The S phase-correlated increase in subunit M2 is regulated by de novo protein synthesis. 609 Apr 44

Rabbits parasitized by Obeliscoides cuniculi were used as models for stomach worm parasitism in ruminants. A 3 X 4 randomized complete block design containing three levels of of infection (NI, no infection; LI and HI, infections produced by 1,800 and 30,000 larvae, respectively) and four levels of diet (PC, high protein and carbohydrate; pc, low protein and carbohydrate; Pc, high protein, and low carbohydrate; pC, low protein and high carbohydrate) was replicated four times. Mean weight gains for rabbits on diets pc or PC were not influenced by infection level, whereas LI rabbits on diets Pc and pC gained as well as the NI animals and more than the HI ones. Only HI rabbits exhibited anorexia. NI and LI rabbits has positive feed conversion efficiencies, whereas those of HI rabbits were negative. The apparent digestibilities of organic matter, protein, and ash in rabbits with different infection levels varied with diet. Daily nitrogen balances were positive. The changes in concentrations of amino acids in the plasma typically associated with systemic, fever-producing infections or with starvation or protein-calorie malnutrition did not occur in infected rabbits. Only the high level infections produced adverse effects on productivity. These effects occurred on diets pc, Pc and pC and were mediated by anorexia.
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PMID:Metabolic effects of infection by the stomach worm Obeliscoides cuniculi in rabbits fed diets varying in nutritive quality. 713 Oct 89

A 3-year 9-month-old child presented unresponsive, dehydrated, and in shock, a consequence of child neglect, abuse, and starvation. This scenario provides the vehicle for a discussion of three problems which can be precipitated by child neglect, specifically kwashiorkor, central pontine myelinolysis, and intellectual repercussions of malnutrition.
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PMID:Altered consciousness and shock in a malnourished child. 888 68

Plants respond to phosphate (Pi) deficiency through adaptive mechanisms involving several morphological, biochemical and molecular changes. In this study, we have characterized the structure and expression of a tomato (Lycopersicon esculentum L.) phosphate starvation-induced gene (TPSI1). A 3.5 kb genomic fragment containing the 474 bp TPSI1 transcript was isolated. The TPSI1 transcript contains an open reading frame of 174 nucleotides encoding a 58 amino acid polypeptide. TPSI1 is an intron-less gene and only one copy could be detected in the tomato genome. The promoter region of TPSI1 contains several conserved sequences found in phosphate starvation induced genes of yeast. The TPSI1 transcripts are rapidly induced in roots and leaves during Pi starvation. A significant increase in the TPSI1 mRNA was observed in cell cultures and roots after 3 and 12 h of Pi starvation, respectively. Induction of the TPSI1 gene appears to be a response specific to Pi starvation since it is not affected by starvation of other nutrients (nitrogen, potassium and iron). The amount of TPSI1 transcript decreased rapidly when Pi-starved tomato plants were resupplied with Pi. These results suggest that TPSI1 gene expression may be a part of the early Pi starvation response mechanism in plants.
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PMID:Differential expression of TPS11, a phosphate starvation-induced gene in tomato. 910 10

In the presence of cefoxitin, which inhibits septum formation during sporulation, Streptomyces griseus is unable to sporulate, retaining the sonication sensitivity of nonsporulating hyphae. Cefoxitin- and sonication-resistant mutant SKK2600 was isolated and showed many morphological differences from its parental strain. A 3.6-kb DNA fragment that complemented the mutations of SKK2600 contained two open reading frames (ORFs), either of which could complement SKK2600. One ORF, designated ssfR, encoded a protein containing a potential DNA-binding helix-turn-helix motif close to its N terminus. SsfR is similar to members of a large family of transcriptional regulators, particularly IclR of Escherichia coli. The second ORF was identified as ssgA, a previously described sporulation gene from S. griseus (S. Kawamoto and J. C. Ensign, Actinomycetology 9:136-151, 1995). A point mutation of C to T seven nucleotides upstream of the UGA stop codon of ssfR was responsible for the phenotype of isolated mutant strain SKK2600. Surprisingly, this mutation should not change the primary structure of SsfR. The ssfR and ssgA disruption mutants were constructed and showed the "white" mutant phenotype, with some growth medium dependence. In addition, the ssfR null mutant sporulated ectopically in phosphate starvation medium.
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PMID:Characterization of ssfR and ssgA, two genes involved in sporulation of Streptomyces griseus. 1098 57

A 3-year-old girl with Graves' disease developed a generalized convulsion as a result of hypoglycemia (25 mg/dL). At the time of the hypoglycemic seizure, her plasma adrenocorticotropin (ACTH) level (1460 pg/mL) was extremely high, but her serum cortisol level (28.4 microg/dL) was relatively low given the severe stress. The cortisol-releasing hormone (CRH) provocation test done after thyroid function had improved revealed normal ACTH and cortisol responses. Since there was no other cause of hypoglycemia, such as hyperinsulinemia, long-term starvation, suddenly advanced emaciation, or prolonged fasting, it was suspected that the transient adrenal hyporesponsiveness was the main cause of hypoglycemia.
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PMID:A 3-year-old girl with Graves' disease with hypoglycemia following transient adrenal hyporesponsiveness. 2230 63


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