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

Goresky, Carl A.; Nadeau, B.

doi:10.1172/jci107598

Cited by 70 publications

(32 citation statements)

References 21 publications

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“…Furthermore, our maximum rate of Dglucose transport is much lower than the data obtained with perfused liver [6,9]. For fructose Sestoft and Fleron [8] obtained a K, of 67 mM with perfused liver and 14 mM with liver cells, which is in contrast to our data.…”

Section: Concentration Dependence Of Hexose Trunsportcontrasting

confidence: 99%

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Transport of Hexoses across the Liver‐Cell Membrane

Baur

Heldt

1977

European Journal of Biochemistry

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The uptake of radioactively labelled hexoses into the cellular space of isolated liver cells has been studied using silicone layer filtering centrifugation. From the hexoses tested, D-glucose is transported most rapidly followed by D-galactose and D-fructose. The rate of L-glucose transport is only 5 % of that of D-glucose. This transport enables the concentration of free aldohexoses in the cellular space to reach the external concentration.For D-glucose the rate of transport into the cell largely exceeds the rate of metabolic conversion. This is different with D-fructose where the rate of transport is considerably lower but the rate of metabolism higher. Here the transport may even be a limiting step.The transport of D-glucose and D-galactose shows a saturation characteristic, whereas D-fructose appears not to be saturatable. The K, for D-glucose is found to be 30 mM. All these hexoses compete with each other for transportation.The temperature dependency of D-glucose reveals an activation energy of 22 kcal (92 kJ)/mol (4-18 "C) and 7 kcal(29 kJ)/mol (18 -37 "C). The transport of D-glucose, D-galactose and D-fructose in inhibited by cytochalasin B, phloretin and phlorizin. It is not dependent on Naf ions. Preliminary results showed no stimulation of the transport by insulin.It is concluded that D-glucose and other hexoses are transported by carrier-mediated diffusion across the plasma membrane of liver cells. This transport shows a large resemblance to the transport of D-glucose into human erythrocytes.It is a long established fact that hexoses permeate the cell membrane of liver very rapidly [2,3]. This led to the conclusion that hexoses enter the liver by free diffusion across the plasma membrane [2-51. On the other hand, it has been reported by Williams et al. [6] that perfused liver takes up D-glucose more rapidly than L-glucose, and that the uptake was inhibited by phloretin. These results indicated the existence of a specific transport system for glucose.Kinetic studies of metabolite transport in perfused liver are very laborious and involve considerable mathematical calculations depending on certain assumptions [7,8]. This may partly explain why the available data on hexose transport in liver are few and variable [5 -101. F.or systematic studies on the kinetics of hexose transport, isolated liver cells may represent a more suitable model. However, it has to be taken into account that by isolating these cells, large areas of the cell membrane which normally are not in contact with the extracellular fluid are exposed to the medium. Furthermore, there is a possibility that transport Parts of these results have been published in a preliminary report [I]. properties may be altered by the isolation procedure, e.g. by treatment with collagenase. Rapid transport of D-fructose into liver cells has been reported recently [8]. Studies from our own laboratory showed that D-glucose was taken up by liver cells more rapidly than D-fructose [Ill. In the present report the properties of hexose transport into liver cells...

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Section: Concentration Dependence Of Hexose Trunsportcontrasting

confidence: 99%

“…[6] (17 mM) but differs largely from the value obtained by Goresky and Nadeau [9] (110 mM). Furthermore, our maximum rate of Dglucose transport is much lower than the data obtained with perfused liver [6,9].…”

Section: Concentration Dependence Of Hexose Trunsportcontrasting

confidence: 56%

Transport of Hexoses across the Liver‐Cell Membrane

Baur

Heldt

1977

European Journal of Biochemistry

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“…2A) showed no evidence of substantial late return of [ 14 C]PLC into the perfusate. If return of [ 14 C]PLC to perfusate occurs, it would have been expected to lead to a downward deviation of the log ratio versus time curve later in time (Goresky and Nadeau, 1974). This behavior was not observed for PLC, which presents an upward straight line constant for the first 16 s (p Ͻ 0.001; r 2 ϭ 0.992; Fig.…”

Section: Discussionmentioning

confidence: 89%

“…A rapid injection (impulse) of labeled test compound (LC or PLC), along with the appropriate reference marker, was made against a range of background concentrations of unlabeled LC or PLC. Because both LC and PLC are nonprotein-bound and low molecular weight substances (Marzo et al, 1991), the reference compound was labeled sucrose, a frequently used marker of the combined vascular space and the space of Disse (Goresky and Nadeau, 1974). C]sucrose were purchased from GE Healthcare (Little Chalfont, Buckinghamshire, UK).…”

mentioning

confidence: 99%

Uptake of l-Carnitine and Its Short-Chain Ester Propionyl-l-carnitine in the Isolated Perfused Rat Liver

Mancinelli

Evans

Nation³

et al. 2005

The Journal of Pharmacology and Experimental Therapeutics

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Hepatic uptake of propionyl-L-carnitine (PLC) and L-carnitine (LC) was assessed with the impulse-response technique in the single-pass perfused rat liver. The experiments involved a rapid injection (impulse) of a mixture of the radiolabeled test compound (PLC or LC) and a reference compound (sucrose) into portal vein inflow and collection and radiochemical analysis (response) of the venous outflowing perfusate samples. The impulse injection was made in the presence of increasing unlabeled background concentrations of PLC (0 -50 M) or LC (50 -500 M) perfusing the liver. The hepatic uptake was minimal or negligible for LC, whereas the hepatic influx clearance was found to be low (0.095 ml/s equivalent to 5.7 ml/min) for PLC relative to the perfusate flow rate (30 ml/min). When background concentrations of PLC were increased (from 1-50 M), the influx clearance was reduced in a concentration-dependent behavior, indicating partial saturation of the entry of compound into hepatocytes. PLC was taken up into hepatocytes via a unidirectional transport process with negligible efflux. The hepatic uptake of PLC was significantly reduced in the presence of unlabeled LC (500 M), indicating an inhibition of the sinusoidal membrane transport of PLC by LC. The study showed the sinusoidal membrane is a permeability barrier to the entry of PLC and LC into hepatocytes, and it is the site of a common carrier-mediated transporter for both compounds.

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“…The carrier demonstrated specificity in that all of the bile acids tested inhibited taurocholate uptake, whereas D-glucose, a substance found not to be actively transported in the liver in vivo (40), did not. Bile acids inhibited only the sodium-dependent portion of taurocholate uptake, whereas BSP inhibited both the sodium-dependent and sodium-independent uptake, suggesting different mechanisms of inhibition for bile acids and BSP.…”

Section: Discussionmentioning

confidence: 98%

Direct determination of the driving forces for taurocholate uptake into rat liver plasma membrane vesicles.

Duffy¹,

Blitzer²,

Boyer³

1983

J. Clin. Invest.

109

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A B S T R A C T To determine directly the driving forces for bile acid entry into the hepatocyte, the uptake of [3H]taurocholic acid into rat liver plasma membrane vesicles was studied. The membrane preparation contained predominantly right-side-out vesicles, and was highly enriched in plasma membrane marker enzymes.The uptake of taurocholate at equilibrium was inversely related to medium osmolarity, indicating transport into an osmotically sensitive space. In the presence of an inwardly directed sodium gradient (NaCl or sodium gluconate), the initial rate of uptake was rapid and taurocholate was transiently accumulated at a concentration twice that at equilibrium (overshoot). Other inwardly directed cation gradients (K+, Li', choline+) or the presence of sodium in the absence of a gradient (Na+ equilibrated) resulted in a slower initial uptake rate and did not sustain an overshoot. Bile acids inhibited sodium-dependent taurocholate uptake, whereas bromsulphthalein inhibited both sodium-dependent and sodium-independent uptake and D-glucose had no effect on uptake. Uptake was temperature dependent, with maximal overshoots occurring at 25°C. Imposition of a proton gradient across the vesicle (pH. < pHj) in the absence of a sodium gradient failed to enhance taurocholate uptake, indicating that Portions of this work were presented at the Annual Meeting of the American Association for the Study of Liver Diseases, 7 November 1981, and published in abstract form: Hepatology (Baltimore),

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

Cited by 70 publications

References 21 publications

Transport of Hexoses across the Liver‐Cell Membrane

Transport of Hexoses across the Liver‐Cell Membrane

Uptake of l-Carnitine and Its Short-Chain Ester Propionyl-l-carnitine in the Isolated Perfused Rat Liver

Direct determination of the driving forces for taurocholate uptake into rat liver plasma membrane vesicles.

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