6-Fluoro-6-deoxy-d-glucose as a tracer of glucose transport

Glucose transport rates are estimated noninvasively in physiological and pathological states by kinetic imaging using PET. The glucose analog most often used is 18F-labeled 2FDG. Compared with glucose, 2FDG is poorly transported by intestine and kidney. We examined the possible use of 6FDG as a tracer of glucose transport. Lacking a hydroxyl at its 6th position, 6FDG cannot be phosphorylated as 2FDG is. Prior studies have shown that 6FDG competes with glucose for transport in yeast and is actively transported by intestine. Its uptake by muscle has been reported to be unresponsive to insulin, but that study is suspect. We found that insulin stimulated 6FDG uptake 1.6-fold in 3T3-L1 adipocytes and azide stimulated the uptake 3.7-fold in Clone 9 cells. Stimulations of the uptake of 3OMG, commonly used in transport assays, were similar, and the uptakes were inhibited by cyclochalasin B. Glucose transport is by GLUT1 and GLUT4 transporters in 3T3-L1 adipocyte and by the GLUT1 transporter in Clone 9 cells. Cytochalasin B inhibits those transporters. Rats were also imaged in vivo by PET using 618FDG. There was no excretion of 18F into the urinary bladder unless phlorizin, an inhibitor of active renal transport, was also injected. 18F activity in brain, liver, and heart over the time of scanning reached a constant level, in keeping with the 6FDG being distributed in body water. In contrast, 18F from 218FDG was excreted in relatively large amounts into the bladder, and 18F activity rose with time in heart and brain in accord with accumulation of 218FDG-6-P in those organs. We conclude that 6FDG is actively transported by kidney as well as intestine and is insulin responsive. In trace quantity, it appears to be distributed in body water unchanged. These results provide support for its use as a valid tracer of glucose transport.

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Hypoxia increases glucose transport at blood-brain barrier in rats

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.2.896 ◽

1994 ◽

Vol 77 (2) ◽

pp. 896-901 ◽

Cited By ~ 72

Author(s):

S. I. Harik ◽

R. A. Behmand ◽

J. C. LaManna

Keyword(s):

Glucose Transport ◽

Blood Brain Barrier ◽

Hypobaric Hypoxia ◽

Cytochalasin B ◽

Bolus Injection ◽

Brain Regions ◽

Brain Barrier ◽

Cerebral Microvessels ◽

Blood Brain

Prolonged hypoxia causes several adaptive changes in systemic physiology and tissue metabolism. We studied the effects of hypobaric hypoxia on glucose transport at the blood-brain barrier (BBB) in the rat. We found that hypoxia increased the density of brain microvessels seen on immunocytochemical stains using an antibody to the glucose transporting protein GLUT. In addition, we found that hypoxia increased the density of GLUT in isolated cerebral microvessels as determined by specific cytochalasin B binding. The higher GLUT density in isolated cerebral microvessels was evident after 1 wk of hypoxia and was associated with decreased activity of gamma-glutamyltranspeptidase. Consistent with these findings, we also demonstrated that 3 wk of hypobaric hypoxia caused increased unidirectional transport of glucose at the BBB in several brain regions in vivo, as determined by the doubly labeled single-pass indicator-fractionation atrial bolus injection method in anesthetized rats. We conclude that chronic hypobaric hypoxia is associated with increased glucose transport at the BBB.

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Rapid regulation of D-glucose transport in basolateral membrane of rat jejunum

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1989.256.5.g878 ◽

1989 ◽

Vol 256 (5) ◽

pp. G878-G883 ◽

Cited By ~ 5

Author(s):

C. I. Cheeseman ◽

D. D. Maenz

Keyword(s):

Glucose Uptake ◽

Glucose Transport ◽

Cytochalasin B ◽

Basolateral Membrane ◽

Membrane Vesicles ◽

Fold Increase ◽

Glucose Infusion ◽

Transport Activity ◽

Site Density

D-Glucose transport and D-glucose inhibitable [3H]cytochalasin B binding to jejunal basolateral membrane vesicles were measured to investigate the possible association between changes in transport activity seen in hyperglycemia and density of transporter sites. Comparison was made between hyperglycemic animals, noninfused rats, and a group infused with sorbitol. Vascular infusion of D-glucose produced a rapid increase in D-glucose transport followed by a delayed and smaller increase in [3H]cytochalasin B binding. The Vmax for glucose uptake was increased after only 30 min of glucose infusion and continued to rise up to 6 h. Comparison with noninfused and sorbitol-infused controls showed that 2 h of glucose infusion produced a 3.5-fold increase in the Vmax for D-glucose uptake while D-glucose-inhibitable binding of [3H]cytochalasin B was unaffected. Six hours of hyperglycemia resulted in the further stimulation of glucose transport (4.1-fold) and a significant 1.8-fold increase in cytochalasin B binding over that for noninfused animals. Vesicles prepared from animals 4 h after an in vivo injection of cycloheximide showed an 80% reduction in glucose transport with no significant change in the cytochalasin B binding density. These results suggest that D-glucose transport in the basolateral membrane is regulated by a combination of a modulation of carriers already in the membrane and subsequent changes in carrier site density.

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Functional expression, quantification and cellular localization of the Hxt2 hexose transporter of Saccharomyces cerevisiae tagged with the green fluorescent protein

Biochemical Journal ◽

10.1042/bj3390299 ◽

1999 ◽

Vol 339 (2) ◽

pp. 299-307 ◽

Cited By ~ 33

Author(s):

Arthur L. KRUCKEBERG ◽

Ling YE ◽

Jan A. BERDEN ◽

Karel van DAM

Keyword(s):

Saccharomyces Cerevisiae ◽

Plasma Membrane ◽

Green Fluorescent Protein ◽

Glucose Transport ◽

Cellular Localization ◽

Fluorescent Protein ◽

Hexose Transporter ◽

High Concentrations ◽

Green Fluorescent

The Hxt2 glucose transport protein of Saccharomyces cerevisiae was genetically fused at its C-terminus with the green fluorescent protein (GFP). The Hxt2-GFP fusion protein is a functional hexose transporter: it restored growth on glucose to a strain bearing null mutations in the hexose transporter genes GAL2 and HXT1 to HXT7. Furthermore, its glucose transport activity in this null strain was not markedly different from that of the wild-type Hxt2 protein. We calculated from the fluorescence level and transport kinetics that induced cells had 1.4×105 Hxt2-GFP molecules per cell, and that the catalytic-centre activity of the Hxt2-GFP molecule in vivo is 53 s-1 at 30 °C. Expression of Hxt2-GFP was induced by growth at low concentrations of glucose. Under inducing conditions the Hxt2-GFP fluorescence was localized to the plasma membrane. In a strain impaired in the fusion of secretory vesicles with the plasma membrane, the fluorescence accumulated in the cytoplasm. When induced cells were treated with high concentrations of glucose, the fluorescence was redistributed to the vacuole within 4 h. When endocytosis was genetically blocked, the fluorescence remained in the plasma membrane after treatment with high concentrations of glucose.

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Glucose transport carrier of human erythrocytes. Radiation-target size of glucose-sensitive cytochalasin B binding protein.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)86179-3 ◽

1980 ◽

Vol 255 (2) ◽

pp. 361-364

Author(s):

C.Y. Jung ◽

T.L. Hsu ◽

J.S. Hah ◽

C. Cha ◽

M.N. Haas

Keyword(s):

Glucose Transport ◽

Cytochalasin B ◽

Binding Protein ◽

Human Erythrocytes ◽

Target Size ◽

Transport Carrier

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Body Composition of Cattle. I. Estimation of Body Fat From Measurement in Vivo of Body Water by Use of Antipyrine

Journal of Applied Physiology ◽

10.1152/jappl.1951.3.11.681 ◽

1951 ◽

Vol 3 (11) ◽

pp. 681-689 ◽

Cited By ~ 30

Author(s):

H. F. Kraybill ◽

O. G. Hankins ◽

H. L. Bitter

Keyword(s):

Body Composition ◽

Body Fat ◽

Body Water

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Acoustoelasticity Analysis of Transient Waves for Non-Invasive In Vivo Assessment of Urinary Bladder

Scientific Reports ◽

10.1038/s41598-018-38445-y ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Mahdi Bayat ◽

Saba Adabi ◽

Viksit Kumar ◽

Adriana Gregory ◽

Jeremy Webb ◽

...

Keyword(s):

Urinary Bladder ◽

Transient Waves ◽

Non Invasive ◽

In Vivo Assessment

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Determination of cerebral glucose transport and metabolic kinetics by dynamic MR spectroscopy

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1997.273.6.e1216 ◽

1997 ◽

Vol 273 (6) ◽

pp. E1216-E1227 ◽

Cited By ~ 6

Author(s):

P. C. M. Van Zijl ◽

D. Davis ◽

S. M. Eleff ◽

C. T. W. Moonen ◽

R. J. Parker ◽

...

Keyword(s):

Glucose Transport ◽

Kinetic Equations ◽

Direct Determination ◽

Life Time ◽

Compartment Model ◽

Brain Extract ◽

Influx Rate ◽

Positron Emission

A new in vivo nuclear magnetic resonance (NMR) spectroscopy method is introduced that dynamically measures cerebral utilization of magnetically labeled [1-13C]glucose from the change in total brain glucose signals on infusion. Kinetic equations are derived using a four-compartment model incorporating glucose transport and phosphorylation. Brain extract data show that the glucose 6-phosphate concentration is negligible relative to glucose, simplifying the kinetics to three compartments and allowing direct determination of the glucose-utilization half-life time [ t ½ = ln2/( k 2 + k 3)] from the time dependence of the NMR signal. Results on isofluorane ( n = 5)- and halothane ( n = 7)- anesthetized cats give a hyperglycemic t ½ = 5.10 ± 0.11 min−1 (SE). Using Michaelis-Menten kinetics and an assumed half-saturation constant Kt = 5 ± 1 mM, we determined a maximal transport rate T max = 0.83 ± 0.19 μmol ⋅ g−1 ⋅ min−1, a cerebral metabolic rate of glucose CMRGlc = 0.22 ± 0.03 μmol ⋅ g−1 ⋅ min−1, and a normoglycemic cerebral influx rate CIRGlc = 0.37 ± 0.05 μmol ⋅ g−1 ⋅ min−1. Possible extension of this approach to positron emission tomography and proton NMR is discussed.

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THE DETERMINATION OF BODY WATER IN VIVO

Nutrition Reviews ◽

10.1111/j.1753-4887.1947.tb04054.x ◽

2009 ◽

Vol 5 (10) ◽

pp. 294-295

Keyword(s):

Body Water

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In vivo total body water assessment by total body electrical conductivity in rats suffering perturbations of water compartment equilibrium

British Journal Of Nutrition ◽

10.1079/bjn19930137 ◽

1993 ◽

Vol 70 (2) ◽

pp. 433-438 ◽

Cited By ~ 7

Author(s):

N. Battistini ◽

F. Virgili ◽

G. Bedogni ◽

G. R. Gambella ◽

A. Bini

Keyword(s):

Electrical Conductivity ◽

Total Body Water ◽

Body Water ◽

Biliary Cirrhosis ◽

Least Squares Regression ◽

Water Compartment ◽

Invasive Method ◽

Total Body ◽

Highly Correlated

Total body electrical conductivity (TOBEC) is a simple and non-invasive method for the assessment of body composition in vivo. Information regarding the applicability of TOBEC in the condition of abnormal fluid balance is scarce. In the present paper we give the results of the comparison between TOBEC and total body water (TBW; assessed by the tritium dilution technique) in three groups of animals: (1) healthy (n 17), (2) expanded fluid volume by secondary biliary cirrhosis (SBC; n 9) and (3) Fiirosemide®-treated rats (n 9). The TOBEC score and TBW by tritium dilution were found to be highly correlated in the pooled sample (r 0·90) and in normal (r 0.·87), SBC (r 0·73) and Furosemide-treated (r 0·89) rats. However, the relationship between TOBEC and TBW, described by least-squares regression analysis, was found to be similar for SBC and normal rats but was significantly different for Furosemide-treated and normal rats. These findings suggest that TOBEC is unable to track TBW accurately when the ratio between intracellular and extracellular water is chronically or acutely altered.

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