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)

Isolated incubated lymphocytes utilized acetoacetate, 3-hydroxybutyrate or oleate at about 0.5 mumol/min per g dry wt. These rates were not markedly affected by concanavalin A or by starvation of the donor animal. When ketone bodies replaced glucose in the culture medium, they could not support lymphocyte proliferation when cells were cultured for 48 h. Addition of oleate (0.5 mM) to isolated lymphocytes increased the rate of O2 consumption markedly, suggesting that it could contribute about 30% to O2 consumption. The rate of oleate uptake and the stimulated rate of O2 consumption were maximal at 0.5 M-oleate; this is in contrast with the effect in some other tissues, in which the rate of fatty acid oxidation is linear with concentration up to about 2 mM. Since the normal plasma concentration of fatty acid in the fed state is about 0.5 mM, this suggests that lymphocytes can utilize fatty acids at a maximal rate in the fed state. Ketone bodies or oleate decreased the rate of glucose utilization by incubated lymphocytes; ketone bodies decreased the rate of pyruvate oxidation and increased the intracellular concentration of hexose monophosphate and citrate, suggesting that 6-phosphofructokinase is inhibited by citrate, and hexokinase by glucose 6-phosphate. These effects may be important not so much in conserving glucose in the whole animal but in maintaining the concentrations of glycolytic intermediates necessary for biosynthetic processes during proliferation.
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PMID:Metabolism of ketone bodies, oleate and glucose in lymphocytes of the rat. 646 15

The effect of diabetes on the metabolism of glucose and lactate was examined in isolated rat cerebral microvessels. In rats with diabetes induced with streptozotocin, glucose oxidation to CO2 by the microvessels was decreased by 54-83% and its conversion to lactate by 21-61%. Insulin therapy for several days or starvation for 48 h both lowered blood glucose levels in the diabetic rats and restored microvessel glucose metabolism to normal. Cerebral microvessels consist principally of the capillaries that constitute the blood-brain barrier. Direct assessment of the blood-brain barrier in vivo using the brain uptake index (BUI) technique revealed a close parallel to the findings in the microvessels. Thus, hexose transport was diminished in diabetic rats and restored to normal by both insulin therapy and starvation. The oxidation of [1-14C]lactate to CO2 like that of glucose was depressed in microvessels of diabetic rats. In contrast to glucose, however, the transport of lactate across the blood-brain barrier in vivo was not altered. These findings suggest that diabetes suppresses glucose metabolism in rat cerebral microvessels and downregulates glucose transport across the blood-brain barrier. They also suggest that both of these processes are regulated by chronic alterations in blood glucose concentration rather than by insulin per se.
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PMID:Diabetes-induced alterations of glucose metabolism in rat cerebral microvessels. 649 67

A close study of the metabolic regulation of hexose transport in a hamster fibroblast mutant, highly defective in the enzyme phosphoglucose isomerase (PGI mutant), reveals the requirement for at least three vectors for transport regulation. The downward regulation of the hexose transport system, called the "transport curb," requires (i) a ligand for the transport system, (ii) oxidative energy metabolism, and (iii) some specific enzymes of the glucose-6-phosphate metabolism. Deprivation of glucose was shown to deprive the PGI mutant of UDP hexose, whereas the glucose-fed mutant contained high levels. The parental strain preserved the UDP hexose with or without glucose feeding. Cycloheximide added to the mutant showed two different types of effects. If added at the onset of glucose starvation, the up-regulation of the transport system was scarcely affected. If cycloheximide was added to the mutant at the onset of glucose refeeding, it prevented the development of the glucose-mediated transport curb. In the mutant, the glucose-mediated curb is not derived from energy metabolism but is solely dependent on certain enzymes of glucose-6-phosphate metabolism. The interference of this curb by cycloheximide requires evidently a reassessment, including that of the role of the UDP hexose pathway in regulation of the hexose transport system.
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PMID:Further clues concerning the vectors essential to regulation of hexose transport, as studied in fibroblast cultures from a metabolic mutant. 658

We used the Oldendorf brain uptake index method to study the blood-brain barrier transport of several metabolic substrates in diabetes. Glucose transport into the brain was decreased by 1/3 in rats with moderate diabetes induced by prior injection of streptozotocin (65 mg/kg of body weight). The transports of mannose and the poorly metabolized hexoses 2-deoxyglucose and 3-O-methylglucose were similarly reduced. Likewise, brain glucose transport was decreased in rats with alloxan-induced diabetes. These alterations in brain hexose influx appeared to be related to chronic (1-2 days) hyperglycemia rather than to insulin-lack per se. Thus, starvation of the diabetic rats for 48 hr restored both the plasma glucose concentration and brain hexose transport to normal. Conversely, the substitution of 10% sucrose for their drinking water both increased plasma glucose and decreased hexose transport in insulin-treated diabetic rats. The 45% decrease in maximal glucose transport rate observed and the uniformity of diminished hexose transport probably imply a decrease in the number of available high-affinity transport carriers at the blood-brain barrier. This defect was specific for hexoses in that the transports of neutral and basic amino acids and of beta-hydroxybutyrate were not similarly affected. These results suggest that chronic hyperglycemia decreases the number of hexose carrier molecules available at the blood-brain barrier. Such an adaptation could operate to decrease the net flux of glucose into the brain during sustained hyperglycemia. It also may explain the abnormal sensitivity to abrupt blood glucose lowering in patients with diabetes mellitus.
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PMID:Metabolic fuel and amino acid transport into the brain in experimental diabetes mellitus. 675 47

We previously reported that growth of influenza virus in the presence of cytochalasin B (CB), a drug that disrupts microfilaments and blocks hexose transport, yields particles with glycoproteins that are heterogeneous and unlabeled by [3H]glucosamine. When the virus was grown in glucose-free medium, we observed reduced virus titers similar to those produced by CB. In contrast, treatment of cells with cytochalasin D (CD) and dihydrocytochalasin B (H2CB), drugs which are known to inhibit microfilament function without affecting hexose transport, did not cause a reduction in virus titers or a change in the electrophoretic mobility of viral glycoproteins. Partial inhibition of glycosylation of viral glycoproteins resulting from either CB-induced inhibition of hexose transport or from glucose starvation resulted in the formation of aggregates of virions on cell surfaces. These aggregates can be dissociated by exogenous neuraminidase. Under these conditions the virions contained a functional hemagglutinin glycoprotein (HA) but an inactive neuraminidase glycoprotein (NA) which was not able to cleave sialic acid, the HA receptor, from viral glycoproteins, or from cellular glycoproteins and glycolipids. Neuraminidase treatment of membrane fractions of CB-treated cells did not cause a shift in the electrophoretic mobility of HA or in the gel elution profile of HA glycopeptides obtained after extensive pronase digestion from HA synthesized in glucose-free medium. These findings suggest that sialic acid is not present on labeled glycoproteins in either of these preparations. We obtained evidence that the sialic acid to which HA binds when NA is inactive is on glycoproteins and glycolipids of cellular origin. Our results support the idea that even when NA is functional, sialylated cellular components impede influenza virus release.
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PMID:Effects of hexose starvation and the role of sialic acid in influenza virus release. 683 15

Regulation of hexose transport was investigated in chicken embryo fibroblasts (CEF) which develop 4- to 8-fold enhanced hexose transport activity during glucose starvation. The presence of cycloheximide in low (0.5 micrograms/ml) concentrations during starvation largely blocked the enhancement of transport activity. Glucose refeeding of CEF in the starvation state led to a decline in transport to the basal level. This decline was either potentiated or blocked by the presence of cycloheximide in low or high (50 micrograms/ml) concentrations, respectively. Exposure of CEF in the fed state to low concentrations of cycloheximide resulted in a 70% decrease of transport within 6 h, whereas exposure to high concentrations of cycloheximide led to only a modest loss (35% decrease). In the glucose-starved state, CEF had no significant decline of transport when exposed to cycloheximide at either high or low concentrations. The uptake of 3-O-methylglucose by fed, starved, or cycloheximide-treated CEF correlated closely with D-glucose transport activity and [3H]cytochalasin B binding by plasma membranes prepared from CEF exposed to the same conditions. Hexose transport activity of CEF seems to largely depend on the number of functioning carriers in the plasma membrane, which apparently reflect the balance between carrier synthesis and inactivation. These two processes require protein synthesis, but are differentially sensitive to the effects of cycloheximide, such that low concentrations of cycloheximide appear to block primarily synthesis while high concentrations block both processes. Furthermore, during starvation the enhancement of transport appears largely due to decreased carrier inactivation in the face of continued carrier synthesis.
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PMID:Regulation of hexose carriers in chicken embryo fibroblasts. Effect of glucose starvation and role of protein synthesis. 688 70

When deprived of D-glucose for 24 hr, chicken embryo fibroblasts exhibit a marked increase in hexose transport activity compared with that of control cells. Scatchard analysis of [3H]cytochalasin B binding to starved cell plasma membranes (46 pmol/mg) indicated a six-fold increase compared with fed cell plasma membranes (7.5 pmol/mg). Irradiation of starved cell plasma membranes with high-intensity UV light in the presence of 0.5 microM [3H]cytochalasin B resulted in covalent labeling of polypeptides of Mr 52,000 and 46,000. In fed cell plasma membranes irradiated under the same conditions, both polypeptides were labeled but at greatly decreased levels. In fact, labeling of the Mr 52,000 polypeptide was barely detectable. The amount of D-glucose-sensitive [3H]cytochalasin B covalent insertion into these membrane components was increased 11 +/- 2 (n = 4)-fold in starved versus fed cell plasma membranes. Photoaffinity labeling of both polypeptides in starved cell plasma membranes was inhibited by D-glucose, 3-O-methylglucose, 2-deoxyglucose, cytochalasin B, and cytochalasin A but not by D-sorbitol, L-glucose, or cytochalasin E. Half-maximal inhibition of labeling of the Mr 52,000 polypeptide occurred at 8 mM D-glucose whereas, for the Mr 46,000 polypeptide, half-maximal inhibition occurred at 40 mM D-glucose. It is concluded that (i) two hexose transport proteins, one of Mr 46,000 and one of Mr 52,000, have been identified in chicken embryo fibroblasts and (ii) the increased affinity labeling of these transporter components after cell starvation may reflect increased numbers of transporters in the plasma membrane.
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PMID:Identification of the stereospecific hexose transporter from starved and fed chicken embryo fibroblasts. 695 40

The effects of starvation for 1, 2 or 3 d and the administration of glucagon to fed rats on the kinetics of active glucose and galactose absorption across the distal ileum have been determined in vivo. Fasting caused reductions in 'apparent Kt' for glucose and galactose transport together with a decrease in Jmax for glucose but not galactose absorption. Treatment with glucagon produced decreases in Kt for the absorption of both hexoses and an increase in Jmax for glucose absorption. The Jmax for galactose uptake, however, was unaltered by glucagon administration. Villus size was unaltered by starvation of up to 3 d duration, but significantly decreased by glucagon treatment. The results suggest that chronically elevated plasma glucagon levels may be a factor in the change in kinetics of hexose absorption in the distal ileum evoked by fasting.
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PMID:Effects of fasting and glucagon on the kinetics of active hexose absorption across the rat distal ileum in vivo. 715 15

1. Changes in the concentrations of the minor constituents of goat's milk were observed during 48 h starvation and on refeeding. 2. The concentrations of hexose phosphate and UDP-hexoses increased during starvation and decreased on refeeding. 3. The concentrations of phosphoenolpyruvate and glycerate 3-phosphate decreased during starvation and increased on refeeding. 4. Isocitrate:2-oxoglutarate increased during starvation and decreased on refeeding. 5. Changes in the minor constituents of milk can be explained in terms of the metabolic changes occurring in the mammary gland during starvation. It is proposed that changes in the concentrations of these metabolites in milk reflect changes in their concentrations in the cytosol or Golgi vesicles of the mammary gland.
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PMID:Changes in the concentrations of the minor constituents of goat's milk during starvation and on refeeding of the lactating animal and their relationship to mammary gland metabolism. 747 Apr 30

Elevated glucose transport rates during glucose deprivation are phenomena that have been observed in several different types of cells in culture. We show here that glucose transport rates in 3T3-L1 adipocytes increased by 10-fold within 18 h in response to glucose deprivation, confirming earlier work by Van Putten and Krans (Van Putten, J. P. M., and Krans, H. M. J. (1985) J. Biol. Chem. 260, 7996-8001). Mannose and 3-O-methylglucose (a nonmetabolizable glucose analog), but not fructose or galactose, blocked the increase in transport activity. Although the increase in transport was dependent on new protein synthesis, only a small and transient increase in GLUT 1 mRNA (less than 2-fold) was observed. In addition, the level of the normal isoform of GLUT 1 (46 kDa) did not increase. A lower molecular mass isoform (37 kDa) was observed but not until 15 h after glucose removal, the appearance of which was clearly not correlated with the increase in activity. Further, the extracellular glucose concentration required to elicit accumulation of this form (p37) was 2 orders of magnitude less than that required for transport stimulation (5 microM versus 500 microM glucose; p37 accumulation and transport activation, respectively). Interestingly, p37 was seen in the presence of galactose, but not fructose, despite elevated transport activity with either sugar. The p37 isoform was slightly larger than N-glycosidase F-treated GLUT 1 (36 kDa), implying that this form is still glycosylated, albeit incompletely. It is not known if p37 is functional, but the time- and sugar-dependent appearance of the lower isoform suggests that p37 is not responsible for starvation-induced transport but potentially represents an underglycosylated precursor of the normal, 46-kDa isoform of GLUT 1.
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PMID:Effect of glucose deprivation of GLUT 1 expression in 3T3-L1 adipocytes. 767 53


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