The exchange of glucose across the liver cell membrane

Studies in rats indicated that the major physiologic stimulus for synthesis of liver glycogen is a rise in the portal glucose concentration after ingestion of a meal. Conversely, glycogen degradation in the liver is stimulated by a rise in portal glucagon concentration. In humans, ingestion of carbohydrate lowers the concentration of circulating glucagon, whereas protein stimulates an increase in peripheral glucagon concentration. Little is known about the effects of these nutrients on glucagon concentrations in the rat. Therefore, we studied the effects of oral protein administration to 24-h-fasted rats pretreated with glucose for 2 h to test the effect of two potent but potentially opposite signals for glycogen metabolism. An increase in liver glycogen concentration was observed in fasted rats given oral glucose, as expected. Removal of glucose by the liver could not account for the glycogen synthesized, indicating that most glycogen formed was derived from gluconeogenesis. In addition, the apparent intracellular and extracellular glucose concentrations were not in equilibrium. A small amount of glucose may have been taken up against a concentration gradient. The portal glucagon was not significantly decreased. Oral protein administration to the rats pretreated with glucose resulted in a rapid and dramatic decrease in liver glycogen concentration. This was associated with an increase in the portal glucagon concentration, no change in insulin concentration, a slight increase in liver cAMP concentration, an increase in the active form of phosphorylase, and a decrease in the active form of synthase. Glycogenolysis could account for the glucose released into the circulation from the liver after protein administration.

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“…The mean ECF fraction of the total liver water was 0.46, which is similar to that reported by Hetenyi et al (29).…”

Section: Icf Fraction = Total Liver Water -Ecf Fractionsupporting

confidence: 90%

Oral Protein Hydrolysate Causes Liver Glycogen Depletion in Fasted Rats Pretreated With Glucose

Gannon

Nuttall

1987

Diabetes

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“…Our modeling of glucose exchange has not taken this additional process into account. We have not incorporated into the modeling the effect of this added flux, the addition of unlabeled glucose to the intracellular space (24). Its addition would complete the modeling so that it would then correspond more accurately to the processes underlying glucose homeostasis.…”

Section: Discussionmentioning

confidence: 99%

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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“…Some non-metabolized analogues of D-glucose, 3-0-methyl glucose and L-glucose, also distribute in a similar intracellular volume (Hetenyi, Norwich, Studney & Hall, 1969). Mediation of monosaccharide transfer by a membrane component is suggested by the finding that L-glucose enters the cells of the isolated perfused liver of the rat very slowly, and that this transfer is inhibited by D-glucose (Williams, Exton, Park & Regen, 1968).…”

Section: Introductionmentioning

confidence: 99%

“…From work with liver slices in vitro (Berthet, Jacques, Hers & DeDuve, 1956) and with perfused rat livers (Hetenyi & Arbus, 1962;Hetenyi, Kopstick & Retelstorf, 1963), it has been concluded that D-glucose equilibrates rapidly between the cell water and the extracellular medium. Some non-metabolized analogues of D-glucose, 3-0-methyl glucose and L-glucose, also distribute in a similar intracellular volume (Hetenyi, Norwich, Studney & Hall, 1969). Mediation of monosaccharide transfer by a membrane component is suggested by the finding that L-glucose enters the cells of the isolated perfused liver of the rat very slowly, and that this transfer is inhibited by D-glucose (Williams, Exton, Park & Regen, 1968).…”

Section: Introductionmentioning

confidence: 99%

The hepatocellular uptake of glucose, galactose and fructose in conscious sheep.

Hooper¹,

Short²

1977

The Journal of Physiology

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Raised blood concentrations of glucose, galactose or Me-a-DG diminished the proportional uptake of D-galactose. Raised blood concentrations of fructose diminished the proportional uptake of fructose.7. Neither total hepatic blood flow changes nor competitive effects within the cell could account for these findings. 8. It is concluded that these monosaccharides enter the liver cell by facilitated diffusion, and share at least some of the membrane elements that mediate this process. It seems likely that only a proportion of the glucose-transporting apparatus is accessible to galactose.

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The exchange of glucose across the liver cell membrane

Cited by 11 publications

References 0 publications

Oral Protein Hydrolysate Causes Liver Glycogen Depletion in Fasted Rats Pretreated With Glucose

Oral Protein Hydrolysate Causes Liver Glycogen Depletion in Fasted Rats Pretreated With Glucose

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

The hepatocellular uptake of glucose, galactose and fructose in conscious sheep.

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