The distribution of glucose and [14C]glucose between erythrocytes and plasma in the rat

1. Of the glucose in rat blood 79.8+/-3.3% (s.d.) was in the plasma. The variance was mostly due to differences between rats. 2. The concentration of glucose in erythrocyte water was 51+/-8% (s.d.) of that in plasma water. 3. The ratio (specific radioactivity in plasma)/(specific radioactivity in whole blood), i.e. the P/B ratio, was estimated for glucose at intervals after intravenous injection of [U-(14)C]glucose and [U-(14)C]fructose. The ratio differed from unity by more than the standard error of a single determination of the specific radioactivity of blood or plasma glucose except from 10 to 17min. after injection of [(14)C]glucose and from 22 to 30min. after injection of [(14)C]fructose. At all other times specific radioactivities in blood had to be corrected to give specific radioactivities in plasma. How to do so is described. 4. The P/B ratios were accounted for by a turnover of glucose in erythrocytes of 0.14mumole/min./ml. of erythrocytes. 5. Metabolism of glucose in rat erythrocytes is unlikely to be a major source of lactate.     

Role of glucose carrier in human erythrocyte water permeability.

Although the transport properties of human erythrocyte water channels have been well characterized, the identity of the protein(s) mediating water flow remains unclear. Recent evidence that glucose carriers can conduct water raised the possibility that the glucose carrier, which is abundant in human erythrocytes, is the water channel. To test this possibility, water permeabilities and glucose fluxes were measured in large unilamellar vesicles (LUV) containing human erythrocyte lipid alone (lipid LUV), reconstituted purified human erythrocyte glucose carrier (Glut1 LUV), or reconstituted glucose carrier in the presence of other human erythrocyte ghost proteins (ghost LUV). In glucose and ghost LUV, glucose carriers were present at 25% of the density of native erythrocytes, were oriented randomly in the bilayer, and exhibited characteristic inhibition of glucose flux when exposed to cytochalasin B. Osmotic water permeability (Pf, in centimeters per second; n = 4) averaged 0.0012 +/- 0.00033 in lipid LUV, 0.0032 +/- 0.0015 in Glut1 LUV, and 0.006 +/- 0.0014 in ghost LUV. Activation energies of water flow for the three preparations ranged between 10 and 13 kcal/mol; p-(chloromercuri)benzenesulfonate (pCMBS), an organic mercurial inhibitor of erythrocyte water channels, and cytochalasin B did not alter Pf. These results indicate that reconstitution of glucose carriers at high density increases water permeability but does not result in water channel activity. However, because the turnover number of reconstituted carriers is reduced from that of native carriers, experiments were also performed on erythrocyte ghosts with intact water channel function. In ghosts, Pf averaged 0.038 +/- 0.013 (n = 9), while the activation energy for water flow averaged 3.0 +/- 0.3 kcal/mol.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationships between blood platelet and erythrocyte formation

The rate of thrombopoiesis was measured by platelet incorporation of ³⁵S-sulfate in mice having markedly stimulated or suppressed erythropoiesis, and compared to controls. Twenty-four hr exposure to 0.4 atm in a low pressure chamber caused increased platelet incorporation of ³⁵S, while exposure for 2 to 5 days caused reductions in both ³⁵S uptake and platelet counts at time of sacrifice. These values were progressively reduced with the longer periods of hypoxia. Two units of human urinary erythropoietin (ESF) were injected twice daily for 1 to 5 days and also caused reduced platelet ³⁵S uptake in mice given the ESF for 2, 4, or 5 days. Mice rendered polycythemic by hypertransfusion or previous exposure to low barometric pressure had increased platelet ³⁵S uptake and increased platelet counts. One possible explanation is that the severe hypoxia or the administration of ESF strongly stimulated erythropoiesis, but might have inhibited thrombopoiesis by depleting megakaryocyte precursors in the bone marrow.     

Changes in relationship between blood glucose level and plasma 1,5-anhydroglucitol level in KK mice

We compared the relationship of the blood glucose level to the plasma 1,5-anhydroglucitol (1,5AG) level between KK mice with abnormal glucose metabolism and ICR mice as controls. Although the plasma 1,5AG level did not show any significant correlation with the blood glucose level in the controls, it tended to logarithmically decrease with the rise in the blood glucose level in KK mice. Thus it is possible that the plasma 1,5AG level is specifically related to the abnormal glucose metabolism in this model of diabetes mellitus and that its routine examination in diabetic patients may help delineate the metabolic derangement in the disease.     

Correlation between plasma growth hormone and insulin and blood glucose concentrations in premature infants.

Plasma growth hormone, insulin and blood glucose levels were measured longitudinally during the first 60 days of life in 21 premature infants (8 males and 13 females) born between the 6th and 8th month of gestation. When these variables were related to age it was found that insulin and glucose, which are lower than in the prepubertal children and adults, rise simultaneously. Whereas growth hormone, which is higher than in older prepubertal children, decreases during the first 2 weeks of life. The decrease in growth hormone continues during the first 2 months of life, in contrast to the increases in insulin and glucose which do not persist in as long a period.     

不同浓度乙醇致小鼠急性酒精中毒与血糖关系的研究

目的研究不同浓度乙醇对小鼠醉酒的影响,筛选益生菌治疗急性酒精中毒的合适的酒精处理浓度,同时研究不同浓度乙醇对小鼠血糖的影响,探究急性酒精中毒程度与血糖的关系。方法将70只昆明小鼠随机分为对照组,乙醇浓度5.0mg/g组、6.0mg/g组、7.0mg/g组、8.0mg/g组、9.0 mg/g组和10.0mg/g组,记录小鼠死亡率并利用血糖仪检测小鼠血糖。根据前期结果,将50只昆明小鼠随机分为乙醇浓度5.5mg/g组、5.8mg/g组、6.1mg/g组、6.4mg/g组和6.7mg/g组,记录小鼠醒酒时间。结果 (1)小鼠在乙醇浓度为6.0、7.0、8.0、9.0和10.0 mg/g时死亡率分别为0%、60%、90%、100%和100%。(2)在乙醇浓度为5.5~6.7mg/g时,随着灌服乙醇浓度的升高,小鼠醒酒时间延长。(3)灌服乙醇浓度越高,小鼠血糖1h时内升高越迅速,1h后降低趋势越明显,7h血糖值低于正常值并持续下降。结论灌服乙醇浓度为6.0mg/g,可以作为合适的益生菌治疗急性酒精中毒模型。急性酒精中毒伴随血糖紊乱,乙醇浓度越高,血糖紊乱越剧烈。     

The basis of echinocytosis of the erythrocyte by glucose depletion

Echinocytosis of erythrocytes by glucose depletion is attributed to adenosine triphosphate depletion, but its process still remains unknown. A mechanism of control of the erythrocyte shape has been previously proposed in which the anion exchanger Band 3, linked to flexible membrane skeleton, has a pivotal role. Recruitments of its inward facing (Band 3(i) ) and outward facing (Band 3(o) ) conformations contract and relax the membrane skeleton, thus promoting echinocytosis and stomatocytosis, respectively. The Band 3(o) /Band 3(i) equilibrium ratio increases with the increase of the Donnan equilibrium ratio, and preferential inward and outward transport by Band 3 of substrates slowly transported are echinocytogenic and stomatocytogenic, respectively. The mechanism suggests the following process. The major organic phosphate 2,3-bisphosphoglycerate is catabolized to lactate to form inorganic phosphate, 3-phosphoglycerate, and adenosine triphosphate. The last two products can be reversibly transformed into 1,3-bisphosphoglycerate and adenosine diphosphate by the glycolytic enzyme phosphoglycerate kinase, thus allowing 2,3-bisphosphoglycerate formation by 2,3-bisphosphoglycerate synthase/phosphatase. The catabolic and cyclic processes initially oppose echinocytosis by increasing the Donnan ratio and outward transport of slowly transported inorganic phosphate by Band 3 (its basic form is transported with a hydrogen ion). Echinocytosis occurs when inward transport of this product becomes predominant. This process can rationalize direct and indirect observations.     

Relationship between the rate of erythrocyte hexose monophosphate pathway and the glucose 6-phosphate concentration

Erythrocytes of individuals with increased (+ 50%) or reduced (-35%) hexokinase activity contain respectively 70 and 17 nmole/ml RBC of glucose-6-phosphate (normal concentration 30 +/- 5nmole/ml RBC) and show comparable rates of the HMP (60 +/- 5nmole/hr/ml RBC). Similarly, in RBC of different ages, obtained by density gradient ultracentrifugation, the glucose-6-phosphate concentration range from 57 (young cells) to 18 (old cells) nmole/ml RBC but the rate at which glucose is utilized in the HMP is unchanged. These data exclude a regulatory role of glucose 6-phosphate in the HMP even if its concentration is under that required for maximal G6PD activity.