Polarity of transport of 2-deoxy-d-glucose and d-glucose by cultured renal epithelia (LLC-PK1)

Miller, John H.; Mullin, James M.; McAvoy, Elizabeth; Kleinzeller, A.

doi:10.1016/0005-2736(92)90361-o

Cited by 28 publications

(23 citation statements)

References 27 publications

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“…The sugar-transporting proteins GLUT 5 and 7 and the sodium-dependent glucose transport proteins SGLT 1 and 2 were not included in our studies because these proteins are known to be either responsible for intestinal (GLUT 5, Burant et al, 1992) or intracellular transport (GLUT 7, Waddell et al, 1992) or transport only glucose but not the glucose analogue FDG that was used in our previous PET analysis (SGLT 1 and 2) (Gould and Holman, 1993;Miller et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Expression of facilitative glucose transport proteins during development of squamous cell carcinomas of the head and neck

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Expression of facilitative glucose transport proteins during development of squamous cell carcinomas of the head and neck

et al. 1999

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“…This change in the molecular structure determines some difference in the biochemical characteristics and in the biologic behavior between glucose and 18 F-FDG. In fact, whereas glucose is completely reabsorbed in the proximal tubules of the kidney, 18 F-FDG is not, resulting in excretion of radioactivity in the urine (1,2). The accumulation of 18 F-FDG activity through the urinary system can be mistaken for focal uptake that is due to oncologic processes, and this physiologic accumulation can interfere with the diagnostic evaluation of the abdominal and pelvic regions even if the patients empty their bladders before the scan (3)(4)(5)(6).…”

mentioning

confidence: 99%

Could Different Hydration Protocols Affect the Quality of 18F-FDG PET/CT Images?

Ceriani

Suriano²,

Ruberto³

et al. 2011

Journal of Nuclear Medicine Technology

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In a group of oncologic patients undergoing 18 F-FDG PET/CT, we compared 4 different protocols of hydration to investigate their impact on image quality and to choose the best practice. Methods: One hundred twenty subjects undergoing 18 F-FDG PET/CT were randomized into 4 groups: group A, receiving free oral hydration; group B, receiving an intravenous injection of 10 mg of furosemide and infusion of 500 mL of saline solution starting 5 min after tracer injection; group C, receiving oral hydration with 500 mL of water; and group D, receiving intravenous injection of 10 mg of furosemide and infusion of 250 mL of the saline solution starting 30 min after the 18 F-FDG injection. The maximum standardized uptake value of muscular and adipose tissues, blood pool (aortic and left ventricular cavity), bladder, and renal parenchyma was calculated for each subject. Results: These 4 groups were comparable in age, body mass index, blood glucose level, and serum creatinine level. Group A showed the worst results. The controlled hydration protocols (groups B, C, and D) provided lower background activity in the soft tissues and lower urinary activity in the bladder and kidney without significant differences in blood activity. The administration of furosemide produces lower activity in the urinary tract without significant changes in 18 F-FDG distribution in the muscle, fat, or blood pool. The best results were in group D. Conclusion: Controlled hydration, particularly with standardized parenteral protocols, reduces the background activity in the soft tissues with the potential benefit of increasing the tumor-to-background contrast. Furosemide does not change tracer distribution in normal tissues but improves the quality of PET/CT images, reducing activity in the excretory system, particularly if the furosemide is administered late after 18 F-FDG injection.

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“…The kilobase values were determined with an RNA ladder (GIBCO BRL) stained with ethidium bromide believed that this membrane component is only present in specialized epithelia such as those from intestine and renal tubules [9,21,[24][25][26] where it participates in transcellular passage of glucose; recent reports, however, have demonstrated that Xenopus oocytes have endogenous co-transporter activity [27,28]. Our studies have shown that the mesangial cell Na+-coupled glucose transporter has close similarities to the carrier from epithelial cells in regard to its specificity of response to the Na + ion, capacity to promote the uptake of (z-methyl-glucoside and inhibition by phlorizin [9,19,21,[24][25][26]. The size of the co-transporte r transcript in the rat mesangial cells (2.2 kb) is similar not only to that of LLC-PK1 cells [21] but also to that reported for rat kidney cortex SGLT1 [29,30].…”

Section: Discussionmentioning

confidence: 57%

“…After exposure of mesangial cells to 20 mmol/1 glucose, a reduction of approximately 70 % in the uptake of c~-methylglucose from that occurring in cells maintained in a glucose concentration of 5 mmol/1 was noted within a 24-h period (Fig. 5); a similar decline in the uptake of 2-deoxyglucose, a specific indicator of facilitated transport [19], was also observed (Fig.5). These observations suggested a down-regulation of both Na+-coupled and facilitative glucose transporters by elevated levels of this sugar.…”

Section: Effect Of Na + On Uptake Of A-methylglucoside By Mesangial Cmentioning

confidence: 75%

“…In order to further evaluate the nature of the carrier systems occurring in mesangial cells, we measured the uptake of the non-metabolizable derivative of glucose, ~-methylglucoside, which is known to utilize the Na+-coupled clucose transporter to effect entrance into the cell [19,20]. A time-dependent uptake of this sugar was observed and this was enhanced in the presence of an increased concentration of NaC1 (Fig.…”

Section: Effect Of Na + On Uptake Of A-methylglucoside By Mesangial Cmentioning

confidence: 99%

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Glucose entry into rat mesangial cells is mediated by both Na+-coupled and facilitative transporters

Wakisaka

Spiro

et al. 1995

Diabetologia

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Summary Since previous studies from our laboratory have demonstrated that increased glucose consumption by cultured rat mesangial cells is accompanied by an accelerated production of type IV and type VI collagen, we have now examined the manner by which glucose is transported into these cells. A progressive stimulation of glucose uptake by the mesangial cells was observed with increasing concentrations of NaC1 so that at 145 mmol/1 about twice as much glucose entered the cells as in its absence (substituted by choline chloride). Moreover, since phlorizin inhibited the NaCl-promoted uptake of glucose and this salt was found to increase the accumulation of c~-methylglucoside in a manner which could not be duplicated by KC1 or mannitol, both Na+-coupled and facilitative glucose transporters appeared to be present in the cells. K m values of 1.93 mmol/1 and 1.36 mmol/1 were determined for the co-transport and facilitated transport pathways, respectively, with their Vma X being 29.5 and 18.0 nmol. mg protein-1.h-1. Both uptake activities were found to be downregulated by exposure of the cells to high glucose and furthermore the Na+-dependent transport could no longer be detected after about 12 passages of the cells. Hybridization of mesangial cell mRNA with cDNA probes revealed transcripts for the Na+/glucose co-transporter as well as GLUT1 and to a lesser extent GLUT4. The identification of the co-transporter in these non-polarized cells is pertinent to an understanding of the intracellular signals which can lead to the development of the diabetic glomerular lesions; in the hyperglycaemic state this carrier provides an additional route for accelerated glucose entry and furthermore by the attendant increase in Na + flux may bring about an alteration in the ionic composition of the cell. [Diabetologia (1995) Although it has become evident that increased deposits of type IV as well as type VI collagen occur in the diabetic glomerulus [4,5] and that mesangial cells in culture demonstrate enhanced production of these two proteins in response to elevated glucose levels [6,7], the mechanism by which glucose and its metabolites regulate the synthesis of the glomerular extracellular matrix remains obscure. Only very limited information is currently available in regard to the manner of entry and subsequent metabolism of glucose by mesangial cells, a subject which is crucial to the understanding of the metabolic hypothesis of diabetic glomerulopathy.In an attempt to fill this void in knowledge and prompted by our recent observation that mesangial

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Polarity of transport of 2-deoxy-d-glucose and d-glucose by cultured renal epithelia (LLC-PK1)

Cited by 28 publications

References 27 publications

Expression of facilitative glucose transport proteins during development of squamous cell carcinomas of the head and neck

Expression of facilitative glucose transport proteins during development of squamous cell carcinomas of the head and neck

Could Different Hydration Protocols Affect the Quality of 18F-FDG PET/CT Images?

Glucose entry into rat mesangial cells is mediated by both Na+-coupled and facilitative transporters

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