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

Studies of glucose transporter activity and anti-glucose transporter (GLUT1) immunoblots were performed on different endothelial cell primary cultures (brain capillary, adrenal capillary and aortic) to determine their response to glucose deprivation. Cell cultures were exposed to glucose deprivation (0.5 mM) for 48 h periods and refed (11.0 mM) for 36 additional hours. Control cultures were kept in 11.0 mM glucose for the duration of these studies. Measurements of 2-[3H]deoxy-D-glucose uptake and membrane fraction purification were performed every 12 h during these timecourses. Baseline cytochalasin-B sensitive uptake of 2-deoxy-D-glucose was near three times larger in brain capillary endothelial cells than in adrenal or aortic endothelial cultures. In all three endothelial cell cultures, 2-deoxy-D-glucose uptake increased during glucose deprivation, and returned to control values upon refeeding. Aortic and adrenal cortical endothelia expressed the starvation induced increases 12 h sooner than brain capillary endothelia. Return to control values was also 12 h faster in these cultured endothelia. Immunoblot studies showed that in all three endothelial cell cultures the increases in transporter activity during glucose starvation correlate with increased membrane expression of GLUT1. Quantitative analysis of the anti-GLUT1 immunoblots indicated that induction of GLUT1 following glucose starvation was slower in brain capillary endothelia than in aortic or adrenal endothelia. The slower response by brain capillary endothelial cells may be related to the higher transport rate of glucose in these cells.
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PMID:Modulation of cultured brain, adrenal, and aortic endothelial cell glucose transport. 897 10

In previous studies we have shown that the insulin-responding glucose transporter isoform of 3T3-L1 adipocytes, GluT4, is almost completely located on microvilli. Furthermore, insulin caused the integration of these microvilli into the plasma membrane, suggesting that insulin-induced stimulation of glucose uptake may be due to the destruction of the cytoskeletal diffusion barrier formed by the actin filament bundle of the microvillar shaft regions [Lange et al. (1990) FEBS Lett. 261, 459-463; Lange et al. (1990) FEBS Lett. 276, 39-41]. Similar shape changes in microvilli were observed when the transport rates of adipocytes were modulated by glucose feeding or starvation. Here we demonstrate that the action of insulin on the surface morphology of hepatocytes is identical to that on 3T3L1 adipocytes; small and narrow microvilli on the surface of unstimulated hepatocytes were rapidly shortened and dilated on top of large domed surface areas. The aspect and mechanism of this effect are closely related to "membrane ruffling" induced by insulin and other growth factors. Pretreatment of hepatocytes with the PI 3-kinase inhibitor wortmannin (100 nM), which completely prevents transport stimulation by insulin in adipocytes and other cell types, also inhibited insulin-induced shape changes in microvilli on the hepatocyte surface. In contrast, vasopressin-induced microvillar shape changes in hepatocytes [Lange et al. (1997) Exp. Cell Res. 234, 486-497] were insensitive to wortmannin pretreatment. These findings indicate that PI 3-kinase products are necessary for stimulation of submembrane microfilament dynamics and that cytoskeletal reorganization is critically involved in insulin stimulation of transport processes. The mechanism of the insulin-induced cytoskeletal reorganization can be explained on the basis of the recent finding of Lu et al. [Biochemistry 35(1996) 14027-14034] that PI 3-kinase products exhibit much higher affinity for the profilin-actin complex than the primary products, PIP and PIP2. Thus, activated PI 3-kinase may direct a flux of profilin-actin complexes to the membrane locations of activated insulin receptors, where, due to the release of actin monomers after binding of profilactin to PI(3,4)P2 and PI(3,4,5)P3, massive actin polymerization is initiated. As a consequence, PI 3-kinase activation initiates a vectorial reorganization of the cellular actin system to membrane sites neighboring activated insulin receptors, giving rise to local membrane stress as visualized by extensive surface deformations and shortening of microvilli. In addition, extensive high-affinity binding of F-actin-barbed endcapping proteins enhances the cytoplasmic concentration of rapidly polymerizing filament ends. Consequently, the actin monomer concentration is lowered and the (cytoplasmic) pointed ends of the microvillar shaft bundle depolymerize and become shorter. The observations presented strengthen the previously postulated diffusion-barrier concept of glucose- and ion-uptake regulation and provide a mechanistic basis for explaining the action of insulin and other growth factors on transport processes across the plasma membrane.
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PMID:Action of insulin on the surface morphology of hepatocytes: role of phosphatidylinositol 3-kinase in insulin-induced shape change of microvilli. 951 32

Functional heterogeneity among pancreatic beta cells is a characteristic feature of the islets of Langerhans. Under physiological conditions, beta cells in the pancreas of fed rats exhibited heterogeneous immunohistochemical staining for insulin and glucokinase. Intracellular beta cell glucokinase staining was either faint or dense. In the pericapillary space beta cell glucokinase immunoreactivity had a polar orientation, with the highest density in cytoplasmic regions close to the blood vessels. Starvation resulted in a loss of heterogeneity with homogeneous insulin staining in all beta cells of the islets, and this was accompanied by a loss of heterogeneous glucokinase staining. The intracellular polarity of glucokinase staining in contact to blood vessels also disappeared after starvation. Refeeding resulted in the reappearance of intercellular heterogeneity. In dependence on the functional demand, the endocrine pancreas recruited insulin from beta cells according to a well-defined hierarchy, with an initial preferential mobilization of medullary beta cells. In the course of this process intracellular polarity of glucokinase staining reappeared in areas of the beta cell with functional contact to the GLUT2 glucose transporter in the plasma membrane. This can be regarded as the morphological correlate of an activation of the glucose signal recognition apparatus. Interestingly, the study also provides evidence that the changes in glucokinase distribution apparently preceded those in insulin distribution, which is in keeping with the central role of glucokinase as the glucose sensor of the pancreatic beta cell.
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PMID:Nutrient-dependent distribution of insulin and glucokinase immunoreactivities in rat pancreatic beta cells. 1007 Dec 39

Mutations in the GSF2 gene cause glucose starvation phenotypes in Saccharomyces cerevisiae. We have isolated the HXT1 gene, which encodes a low-affinity, high-capacity glucose transporter, as a multicopy suppressor of a gsf2 mutation. We show that gsf2 mutants accumulate Hxt1p in the endoplasmic reticulum (ER) and that Gsf2p is a 46-kDa integral membrane protein localized to the ER. gsf2 mutants also display a galactose growth defect and abnormal localization of the galactose transporter Gal2p but are not defective in function or localization of the high-affinity glucose transporter Hxt2p. These findings suggest that Gsf2p functions in the ER to promote the secretion of certain hexose transporters.
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PMID:Efficient export of the glucose transporter Hxt1p from the endoplasmic reticulum requires Gsf2p. 1037 29

Initial attempts to increase fermentative capacity of baker's yeast focussed on the overproduction of single enzymes, which proved to be insufficient. Nowadays many components of the system are monitored simultaneously in a search for a correlation with fermentative capacity. However, this strategy has not yet proven fruitful either. Here we investigate an element previously neglected, the glucose transporter, and find that a loss of glucose transport capacity correlates with a decrease of fermentative capacity during nutrient starvation. However the correlation is not unique, suggesting that the loss of fermentative capacity cannot be attributed to an inactivation of glucose transport alone. Our results suggest the necessity to use a detailed kinetic model as an underlying working hypothesis and to use Metabolic Control Analysis to examine the pathway's control properties.
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PMID:Loss of fermentative capacity in baker's yeast can partly be explained by reduced glucose uptake capacity. 1224 Oct 67

We have investigated the role and the kinetic properties of the Hxt5 glucose transporter of Saccharomyces cerevisiae. The HXT5 gene was not expressed during growth of the yeast cells in rich medium with glucose or raffinose. However, it became strongly induced during nitrogen or carbon starvation. We have constructed yeast strains constitutively expressing only Hxt5, Hxt1 (low affinity) or Hxt7 (high affinity), but no other glucose transporters. Aerobic fed-batch cultures at quasi steady-state conditions, and aerobic and anaerobic chemostat cultures at steady-state conditions of these strains were used for estimation of the kinetic properties of the individual transporters under in vivo conditions, by investigating the dynamic responses of the strains to changes in extracellular glucose concentration. The K(m) value and the growth properties of the HXT5 single expression strain indicate that Hxt5 is a transporter with intermediate affinity.
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PMID:Determination of in vivo kinetics of the starvation-induced Hxt5 glucose transporter of Saccharomyces cerevisiae. 1270 77

Using a differential display technique, the gene gtt1, which codes for a high-affinity glucose transporter, has been cloned from the mycoparasite fungus Trichoderma harzianum CECT 2413. The deduced protein sequence of the gtt1 gene shows the 12 transmembrane domains typical of sugar transporters, together with certain residues involved in glucose uptake, such as a conserved arginine between domains IV and V and an aromatic residue (Phe) in the sequence of domain X. The gtt1 gene is transcriptionally regulated, being repressed at high levels of glucose. When carbon sources other than glucose are utilized, gtt1 repression is partially alleviated. Full derepression of gtt1 is obtained when the fungus is grown in the presence of low carbon source concentrations. This regulation pattern correlates with the role of this gene in glucose uptake during carbon starvation. Gene expression is also controlled by pH, so that the gtt1 gene is repressed at pH 6 but not at pH 3, a fact which represents a novel aspect of the influence of pH on the gene expression of transporters. pH also affects glucose transport, since a strongly acidic pH provokes a 40% decrease in glucose transport velocity. Biochemical characterization of the transport shows a very low K(m) value for glucose (12 micro M). A transformant strain that overexpresses the gtt1 gene shows a threefold increase in glucose but not galactose or xylose uptake, a finding which confirms the role of the gtt1 gene in glucose transport. The cloning of the first filamentous ascomycete glucose transporter is the first step in elucidating the mechanisms of glucose uptake and carbon repression in aerobic fungi.
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PMID:Glucose uptake in Trichoderma harzianum: role of gtt1. 1291 90

Fungi employ different carbohydrate uptake systems to adapt to certain environmental conditions and to different carbon source concentrations. The hydrolysis of polymeric carbohydrates and the subsequent uptake of monomeric forms may also play a role in development. Aspergillus nidulans accumulates cell wall components during vegetative growth and degrades them during sexual development. We have identified the hxtA (high affinity hexose transporter) gene in a differential library, which was enriched for sexual-specific genes. The hxtA gene is disrupted by 6 introns and predicted to encode a 531 amino acid protein with high similarity to major facilitator superfamily members including the high affinity hexose transporter Gtt1 from Trichoderma harzianum. A. nidulans HxtA contains the 12 predicted transmembrane domains characteristic for this family. Deletion of hxtA did not impair growth of A. nidulans on a variety of carbon sources nor did it inhibit sexual development suggesting redundant sugar uptake systems. We found at least 17 putative hexose transporters in the genome of A. nidulans. Despite the high similarity of HxtA to fungal high affinity glucose transporters, the hxtA gene did not restore growth on glucose of a Saccharomyces cerevisiae mutant, in which all hexose transporters were deleted. Northern blot analysis revealed that the A. nidulans hxtA gene was repressed under high glucose conditions and expressed in vegetative hyphae upon carbon starvation and during sexual development. We found hxtA(p)::sgfp expression in developing cleistothecia specifically in ascogenous hyphae and propose that HxtA is a high affinity glucose transporter involved in sugar metabolism during sexual development.
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PMID:A putative high affinity hexose transporter, hxtA, of Aspergillus nidulans is induced in vegetative hyphae upon starvation and in ascogenous hyphae during cleistothecium formation. 1473 61

A putative glucose transporter, GLUT1, is reported for Atlantic cod Gadus morhua. A combination of RT-PCR, RLM-RACE and genome walking were used to articulate a 4560 bp cDNA (GenBank accession number AY526497). It contains a 149 bp 5' UTR, a 1470 bp open reading frame and a 2941 bp 3' UTR. At the nucleotide level, the cod GLUT1 ORF shares 78.2% sequence identity to human GLUT1 and the deduced amino acid sequence clusters with GLUT1s from rainbow trout and carp. GLUT1 transcript is highly expressed in brain, gill, heart and kidney and expressed to a lower level in at least six other tissues. Expression is evident immediately upon fertilization of eggs. Six hours of hypoxia at 40% DO(2) did not alter expression levels in brain, gill, heart or kidney. The level of expression is not substantially altered in heart during low temperature challenge, although there is a suggestion that colder temperature could lead to lower levels of expression, consistent with the concept that the cold-acclimated heart has a reduced dependence upon glucose as a metabolic fuel. Two months of starvation did not significantly alter the level of expression of GLUT1 in heart. This is in marked contrast to the rat heart where fasting leads to a substantial decrease in GLUT1 levels. Overall, there is a ubiquitous tissue distribution of GLUT1, consistent with other species, and the level of gene expression, especially in heart, is relatively constant over a range of physiological conditions.
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PMID:Sequence and expression of a constitutive, facilitated glucose transporter (GLUT1) in Atlantic cod Gadus morhua. 1557 63

SEN1 is a senescence-associated gene in Arabidopsis which is strongly induced by phosphate (Pi) starvation. To investigate the interaction between Pi starvation induced regulation system and senescence-induced regulation system, SEN1 promoter-glucuronidase (GUS) chimeric gene was constructed into the pCAMBIA1391z plasmid. The promoter region of the SEN1 was investigated by PCR amplification. The expression of SEN1 gene in leaves was enhanced under nutrition stress (nitrogen, phosphate, and potassium starvation), but the expression of SEN1 gene in roots was induced only by phosphate starvation. SEN1 was induced in elongated hypocotyl in darkness, suggesting that SEN1 may involved in light-regulated hypocotyl elongation. Fluorometric assays of the GUS activity indicate that the expression of SEN1 induced by phosphate starvation was repressed by addition of glucose and cytokinin, which indicates that Pi-starvation signaling on SEN1 may overlap with the Pi-signaling on other Pi-starvation response genes. Expression of the SEN1 gene was also strongly induced in leaves and roots by 3% glucosamine, a inhibitor of glucose transporter under both Pi sufficient and deficient conditions, while cytokinin reduced the expression under Pi starvation condition, but not under Pi sufficient condition. The results provide clues that the up-regulated expression of SEN1 by glucosamine give rise to glucose limitation through a signaling pathway regulated by Pi starvation. The cis-acting elements distributed in the promoter of SEN1 has also been discussed.
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PMID:[The effects of phosphorus, glucose and cytokinin on SEN1 gene expression in Arabidopsis]. 1569 83


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