The distribution of glucose and methyl-glucose between the liver and plasma in normal and insulin injected rats

Hetenyi, G; Studney, D. R.

doi:10.1007/bf02136299

Cited by 15 publications

(8 citation statements)

References 10 publications

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“…The extracellular compartment has been reported to be -3 0 % of total liver water. 27 We have obtained similar data (unpublished observations). Therefore, the mean ICF concentrations in fasted rats were calculated from the measured liver and plasma water concentrations as follows: Measured liver concentration (micromoles per milliliter total liver water) = 0.7 (ICF) + 0.3 (ECF).…”

Section: Methodssupporting

confidence: 88%

“…In addition, because not all liver water may be accessible, concentrations per milliliter available intracellular water may be higher. 27 The concentrations of hepatic metabolites and enzymes (which are entirely intracellular and thus are not being compared with plasma concentrations) are given in micromoles per gram wet weight or units per gram wet weight to facilitate comparison with literature values. These concentrations can be converted to micromoles per milliliter intracellular liver water (ICF) by dividing by 0.49.…”

Section: Methodsmentioning

confidence: 99%

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Mechanism of Stimulation of Liver Glycogen Synthesis by Fructose in Alloxan Diabetic Rats

Niewoehner

Nuttall

1986

Diabetes

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In diabetic animals and humans, stimulation of liver glycogen synthesis has been reported after administration of a large parenteral fructose load. The effects of an oral fructose load have not been examined previously. In the diabetic state, glycogen synthase phosphatase activity is reduced, and synthase D (the inactive form) is a poor substrate for the phosphatase. Thus, activation of synthase to the synthase R and synthase I (R + I) (active) forms by fructose would not be expected. We have determined that oral fructose administration does stimulate glycogen synthesis and have examined the mechanism by which this is accomplished. In 24-h-fasted alloxan diabetic rats, basal liver glycogen was higher than in normal rats (8.3 +/- 1.8 vs. 3.0 +/- 0.5 mg/g wet wt). After fructose (4 g/kg) was given, the initial rate of glycogen synthesis was normal in diabetic rats, but total glycogen synthesis was reduced. By 240 min, liver glycogen increased to 18 +/- 4.0 mg/g wet wt in diabetic rats versus 30.5 +/- 1.5 mg/g wet wt in normal rats. Synthase R + I was low and did not increase significantly (0.063 +/- 0.006 to 0.064 +/- 0.010 U/g wet wt) after fructose administration to the diabetic animals. Phosphorylase a did not decrease significantly during the period of active glycogen synthesis. In the diabetic rats, glucose-6-phosphate increased by 84% (0.103 +/- 0.010 to 0.184 +/- 0.020 mumol/g wet wt) within 10 min and remained elevated above the control level. UDPglucose decreased from 0.336 +/- 0.013 to 0.271 +/- 0.011 mumol/g wet wt at 10 min and remained below the control level.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Methodssupporting

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Mechanism of Stimulation of Liver Glycogen Synthesis by Fructose in Alloxan Diabetic Rats

Niewoehner

Nuttall

1986

Diabetes

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“…The comparison of plasma and liver solute concentrations should be based on concentrations in plasma and liver water. Plasma is 94% water by weight; liver is 70% water (22,23). We have confirmed this in freeze-clamped liver in our laboratory.…”

Section: Methodssupporting

confidence: 76%

“…We have assumed linear extracellular metabolite concentrations across the liver although hepatocellular-to-plasma gradients may not be uniform (25)(26)(27). In addition, because not all liver water may be accessible, concentrations per milliliter available intracellular water may be even higher (22).…”

Section: Methodsmentioning

confidence: 99%

Relationship of Hepatic Glucose Uptake to Intrahepatic Glucose Concentration in Fasted Rats After Glucose Load

Niewoehner

Nuttall²

1988

Diabetes

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Glucose concentration gradients across the liver and hepatic blood flow were measured to characterize the relationship of hepatic glucose uptake to hepatic glucose concentration for 240 min after administration of a large oral glucose load to fasted rats. Extraction of glucose occurred only transiently, from 20 to 80 min after glucose administration. The liver changed from net glucose output to net glucose removal only when the intracellular hepatic glucose concentration exceeded 12.5 mumol/ml water. Even when arteriovenous glucose concentrations gradients were compatible with net direct hepatic uptake of glucose, the hepatic glucose concentration always exceeded the inflow glucose concentration. These data indicate that direct glucose uptake occurred against a concentration gradient when the liver is considered as a whole. The hepatic intracellular-to-extracellular glucose concentration gradient changed very little, suggesting that this is not being regulated by glucose, insulin, or other effectors. The mechanism by which the hepatic glucose concentration and net hepatic glucose uptake versus output are coordinated is unknown. The rate of glycogen synthesis was linear for 120 min after administration of the glucose load. This occurred in the presence of direct uptake of glucose early in the time course and later in the presence of net glucose output by the liver. Net direct uptake of glucose by the liver could account for, at most, 37-55% of the glycogen formed. Fractional extraction of both lactate and alanine decreased after glucose was given, but net hepatic uptake of these metabolites could account for 33-49 and 7-10%, respectively, of the glycogen formed, depending on plasma versus blood water flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Blood glucose was determined by means of a glucose oxidase method using a Beckman glucose analyzer (Fullerton, CA), whereas hepatic tissue glucose was determined spectrophotometrically by the method of Bergmeyer et al (4), using hexokinase and glucose-6-phosphate dehydrogenase. The liver glucose concentration was measured directly and calculated using total liver water as the denominator on the basis of a report that the extracellular component is ϳ30% of the liver water, whereas the intracellular component is 70% (11,26). Plasma insulin was measured using a speciesspecific double-antibody radioimmunoassay (Phadeseph Insulin Test; Pharmacia Diagnostics, Uppsala, Sweden) and the plasma glucagons with a commercially available kit (Daiichi, Tokyo, Japan), with interassay coefficients of variability of 11 and 8%, respectively.…”

Section: Methodsmentioning

confidence: 99%

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

Ogihara¹,

Kawamura²,

Kasuga³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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To characterize the "portal signal" during physiological glucose delivery, liver glycogen was measured in unrestrained rats during portal (Po) and peripheral (Pe) constant-rate infusion, with minimal differences in hepatic glucose load (HGL) and portal insulin between the delivery routes. Hepatic blood flows were measured by Doppler flowmetry during open surgery. Changes in hepatic glucose, portal insulin, glucagon, lactate, and free fatty acid concentrations were generally similar in either delivery except for glucagon at 4 h. Hepatic glycogen, however, increased continuously in Po and was higher than Pe at 8 and 24 h, although it decreased to the level of Pe upon the removal of Po at 8 h. There was a near-linear relationship between hepatic glycogen and HGL in either delivery, with the slope being twice as high in Po and the intercepts converging to basal HGL. The hepatic response to Po did not alter upon 80% replacement by Pe. These results suggest that negative arterial-portal glucose gradients increase the rate of hepatic glycogen synthesis against the incremental HGL in an all-or-nothing mode.hepatic glycogen synthesis; hepatic glucose load; negative arterialportal glucose gradients; nonsteady state IT HAS BEEN WELL DOCUMENTED that portal glucose delivery (Po) creates an important signal to enhance net hepatic glucose uptake (NHGU) or hepatic glycogen deposition in rodents (6, 9, 33), dogs (1-3, 14, 24, 25, 29 -31), and humans (8). Evidence has shown that NHGU is dependent on hepatic glucose load (HGL), plasma insulin concentration, and negative arterial-portal (A-P) glucose gradients. Adkins et al. (1) and have shown that a negative A-P gradient might serve as the portal signal, whereas Pagliassotti et al. (31) found that the magnitude of NHGU is dependent on the magnitude of the A-P gradients. On the other hand, Myers and colleagues (24,25) demonstrated that NHGU is linearly related to HGL, whereas it is curvilinearly related to the plasma insulin concentration, and that the hepatic response to Po results in a leftward shift in the dose-response relationship. These results have been obtained under hyperglycemic hyperinsulinemic and/or pancreatic clamp conditions, where the concentration of plasma glucose, that of insulin, or the negative A-P gradients were varied while the other two conditions were held fixed. Therefore, the relationship within these parameters remains unsettled in the nonsteady hyperglycemic state. Moore et al. (22) showed that, even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to stimulate NHGU during glucose infusion at a constant rate in dogs. In a similar experiment, we (28) also observed that there was a linear relationship between NHGU and HGL in either method of delivery, with the slope being four times steeper in Po and the HGL intercepts converging to near-basal values. We hypothesized from these results that the portal signal might increase the slope for NHGU against HGL.Therefore, the aim of the present study was to prove the hypo...

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The distribution of glucose and methyl-glucose between the liver and plasma in normal and insulin injected rats

Cited by 15 publications

References 10 publications

Mechanism of Stimulation of Liver Glycogen Synthesis by Fructose in Alloxan Diabetic Rats

Mechanism of Stimulation of Liver Glycogen Synthesis by Fructose in Alloxan Diabetic Rats

Relationship of Hepatic Glucose Uptake to Intrahepatic Glucose Concentration in Fasted Rats After Glucose Load

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

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