Stereospecific transport of glucose in the perfused rat liver

Tf, Williams; Jh, Exton; Cr, Park; Regen, DM

doi:10.1152/ajplegacy.1968.215.5.1200

Cited by 123 publications

(55 citation statements)

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“…This is not very surprising, if we consider that, in their experiments, Williams et al (6) were unable to demonstrate measurable amounts of labeled phosphorylated intermediates by mixed bed resin Exchange of Glucose across Liver Cell Membranes extraction of deproteinized extracts of liver, obtained 2 ing equal to zero. Optimized values for the four pamin after beginning a steady infusion of labeled D-glu-rameters ay, to, k2, and kio/(l + Y) were determined.…”

Section: Resultsmentioning

confidence: 93%

“…We selected labeled sucrose as an appropriate extracellular reference, a substance which is not transported. In the isolated perfused liver, it is completely excluded from the liver cells (6). In the intact animal, the apparent volume of distribution of labeled sucrose in the liver increases slowly, as a result of the hydrolysis and reabsorption (as monosaccharide) of the small amounts secreted in bile (16).…”

Section: Discussionmentioning

confidence: 99%

“…In 1967, we examined tracer D-glucose entry into the intact liver, by means of the multiple indicator dilution technique, and reported qualitatively that raising the plasma glucose levels slowed the relative rate of entry of tracer D-glucose and that the rate of entry of tracer L-glucose was very slow (5). Simultaneously Williams, Exton, Park, and Regen explored the entry process, utilizing the isolated perfused liver (6). They showed, by tissue sampling, that although equilibration within the liver cells of D-glucose (tracer and load) occurs within 10 min, the process is incomplete in 2 min, and tracer L-glucose enters liver cells, but equilibrates only over a period of approximately 40 min.…”

Section: Introductionmentioning

confidence: 99%

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Uptake of materials by the intact liver. The exchange of glucose across the cell membranes.

Goresky

Nadeau²

1974

J. Clin. Invest.

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A B S T R A C T D-Glucose equilibrates within liver cells.We have studied its process of entry into and exit from these cells with the multiple indicator dilution technique. Labeled red cells (a vascular indicator), labeled sucrose (an extracellular reference), and labeled D-glucose were rapidly injected into the portal vein, and from serially sampled hepatic venous blood, normalized outflow-time patterns were obtained. The labeled red cell curve rises to an early high peak, and decays rapidly; and that for sucrose reaches a later and lower peak and decays less rapidly, but generates an equivalent area. The curve for labeled D-glucose begins with that for labeled sucrose, gradually rises to a peak which is later and substantially lower than that for sucrose, and then decreases slowly. At high glucose levels this curve assumes a squared-off shape, rises fairly quickly to its highest level, at the time of the sucrose peak, and then slowly decreases. Phlorizin and galactose infusion result in the emergence of a pronounced early peak, under the sucrose peak; and the curve for tracer L-glucose approaches that for sucrose.

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Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Uptake of materials by the intact liver. The exchange of glucose across the cell membranes.

Goresky

Nadeau²

1974

J. Clin. Invest.

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“…Overexpression of the facilitative glucose-transporter has been observed for a wide range of human cancers (41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58) with the degree of overexpression generally being inversely correlated with prognosis. The mechanisms by which GLUTs promote malignant cellular behaviour have focused on factors inducing its expression, such as local hypoxia (37), oncogenes such as Ras, Scr (15) or Myc (38).…”

Section: Discussionmentioning

confidence: 99%

Fructose transporter Glut5 expression in clear renal cell carcinoma

Villaamil

Gallego²,

Rubira³

et al. 2011

Oncol Rep

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Abstract. Renal cell carcinomas (RCC) can be subclassified for general purposes into clear cell, papillary cell, chromophobe cell carcinomas and oncocytomas. Other tumours such as collecting duct, medullary, mucinous tubular and spindle cell and associated with Xp 11.2 translocations/TFE 3 gene fusion, are much less common. There is also a residual group of unclassified cases. Previous studies have shown that RCC has high glycolytic rates, and expresses GLUT transporters, but no distinction has been made among the different subtypes of renal cell tumours and their grades of malignancy. In clear renal cell carcinoma (cRCC) glycogen levels increase, glycolysis is activated and gluconeogenesis is reduced. The clear cell subtype of RCC is characterized histologically by a distinctive pale, glassy cytoplasm and this appearance of cRCC is due to abnormalities in carbohydrate and lipid metabolism, and this abnormality results in glycogen and sterol storage. Several isoforms of glucose carriers (GLUTs) have been identified. We show here in a panel of 80 cRCC samples a significant correlation between isoform 5 (GLUT5) and many pathological parameters such as grade of differentiation, pelvis invasion and breaking capsule. GLUT5 expression also appears to associate more strongly with the clear cell RCC subtype. These data suggest a role for the GLUT5 isoform in fructose uptake that takes place in cRCC cells and which subsequently leads to the malignant RCC progression.

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“…Such a mechanism appears to be provided by insulin acting on pyruvate dehydrogenase phosphate phosphatase. The (Cahill et al, 1958;Williams et al, 1968), and apparently the increased flux through pyruvate dehydrogenase needed for lipogenesis is accomplished simply via elevations in liver pyruvate concentrations (Patzelt et al, 1973). Severson et al (1974) were unable to observe any action of insulin on pyruvate dehydrogenase phosphate phosphatase activity and their results thus differ from the present finding and the earlier report of Sica & Cuatrecasas (1973).…”

Section: Discussionmentioning

confidence: 99%

Activation of pyruvate dehydrogenase in adipose tissue by insulin. Evidence for an effect of insulin on pyruvate dehydrogenase phosphate phosphatase

Mukherjee

Jungas

1975

Biochemical Journal

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1. The mechanism by which insulin activates pyruvate dehydrogenase in rat epididymal adipose tissue was further investigated. 2. When crude extracts, prepared from tissue segments previously exposed to insulin (2m-i.u/ml) for 2min, were supplemented with Mg-2+, Ca-2+, glucose and hexokinase and incubated at 30 degrees C, they displayed an enhanced rate of increase in pyruvate dehydrogenase activity compared with control extracts. 3. When similar extracts were instead supplemented with fluoride, ADP, creatine phosphate and creatine kinase, the rate of decrease in pyruvate dehydrogenase activity observed during incubation at 30 degrees C was unaffected by insulin treatment. 4. It is suggested that insulin increases the fraction of pyruvate dehydrogenase present in the tissue in the active dephospho form by increasing the activity of pyruvate dehydrogenase phosphate phosphatase.

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Stereospecific transport of glucose in the perfused rat liver

Cited by 123 publications

References 0 publications

Uptake of materials by the intact liver. The exchange of glucose across the cell membranes.

Uptake of materials by the intact liver. The exchange of glucose across the cell membranes.

Fructose transporter Glut5 expression in clear renal cell carcinoma

Activation of pyruvate dehydrogenase in adipose tissue by insulin. Evidence for an effect of insulin on pyruvate dehydrogenase phosphate phosphatase

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