The effect of worm, age, weight and number in the infection on the absorption of glucose by Hymenolepis diminuta

Parasitology ◽  
1977 ◽  
Vol 75 (3) ◽  
pp. 277-284 ◽  
Author(s):  
D. Henderson

SummaryIn Hymenolepis diminuta the in vitro rate of absorption of glucose/unit dry weight of worm falls with increasing worm age, with increasing worm weight and as the number of worms in an infection is increased. In a 6 mM solution of glucose, a 5 mg (dry weight) worm from a 7 or 8 worm infection absorbed 80 µmoles/g dry weight/5 min whereas a 60 mg worm, also from a 7 or 8 worm infection, absorbed only 35µmoles/g dry weight/5 min. This change in the rate of absorption is, at least partly, thought to be due to changes in the relative surface area: weight ratio during growth of the worm.The kinetic parameter, Kt glucose, increased from 1.1 mM for a 5 mg (dry weight) worm from a 7 or 8 worm infection to 2 mM for a 60 mg worm. This change in the functioning of the glucose transport system may indicate that there are two components of the glucose transport system – or two separate systems – one with a low Kt and one with a high Kt, the ratios of which change during worm growth.The smaller the number of worms in an infection the greater the rate of glucose absorption. Using 8–day–old worms in a 6 mM glucose solution, 1 worm from a single worm infection absorbs 111 μmoles/g dry weight/5 min, 1 worm from a 7 or 8 worm infection absorbs 88 μmoles/g dry weight/5 min and 1 worm from a 45–50 worm infection absorbs 77 μmoles/g dry weight/5min. The significance of this is discussed with reference to the ‘crowding effect’ in tapeworms.

1993 ◽  
Vol 39 (7) ◽  
pp. 722-725 ◽  
Author(s):  
John L. Wylie ◽  
Elizabeth A. Worobec

Specificity of the high-affinity glucose transport system of Pseudomonas aeruginosa was examined. At a concentration of [14C]glucose near the Vmax of the system, inhibition by maltose, galactose, and xylose was detected. This inhibition is similar to that detected in earlier in vivo studies and correlates with the known specificity of OprB, a glucose-specific porin of P. aeruginosa. At a level of [14C]glucose 100 times lower, only unlabelled glucose inhibited uptake to any extent. This matches the known in vitro specificity of the periplasmic glucose binding protein. These findings were used to explain the discrepancy between earlier in vivo and in vitro results reported in the literature.Key words: Pseudomonas aeruginosa, glucose transport, OprB, glucose binding protein.


1990 ◽  
Vol 122 (5) ◽  
pp. 585-591 ◽  
Author(s):  
Christiane Prager ◽  
Heide S. Cross ◽  
Meinrad Peterlik

Abstract. The possible contribution of increased D-glucose absorption from the intestine to the impairment of oral glucose tolerance in hyperthyroidism was evaluated by investigating the influence of T3 on different pathways of D-glucose transport, utilizing an organ culture system of embryonic chick small intestinal explants. T3, when present in the culture medium at a concentration between 10−10-10−8 mol/l, had no effect on uptake of α-methyl-D-glucoside, but stimulated uptake of 2-deoxy-D-glucose by the intestinal epithelium in a dose-dependent fashion. T3 thereby enhanced the maximal velocity of a saturable, cytochalasin B-sensitive but phloretin-insensitive 2-deoxy-D-glucose transport system with an apparent Km of 7 mmol/l. The combined data are consistent with the assumption that T3 can enhance D-glucose entry into the intestinal epithelium through stimulationof a low-affinity transport system at the brush-border membrane of enterocytes. Our findings provide a basis for the explanation of adaptive modulation of intestinal glucose absorption in hyperthyroidism.


1999 ◽  
Vol 342 (2) ◽  
pp. 321-328 ◽  
Author(s):  
Jeffrey W. RYDER ◽  
Yuichi KAWANO ◽  
Alexander V. CHIBALIN ◽  
Jorge RINCÓN ◽  
Tsu-Shuen TSAO ◽  
...  

We have characterized the glucose-transport system in soleus muscle from female GLUT4-null mice to determine whether GLUT1, 3 or 5 account for insulin-stimulated glucose-transport activity. Insulin increased 2-deoxyglucose uptake 2.8- and 2.1-fold in soleus muscle from wild-type and GLUT4-null mice, respectively. Cytochalasin B, an inhibitor of GLUT1- and GLUT4-mediated glucose transport, inhibited insulin-stimulated 2-deoxyglucose uptake by > 95% in wild-type and GLUT4-null soleus muscle. Addition of 35 mM fructose to the incubation media was without effect on insulin-stimulated 3-O-methylglucose transport activity in soleus muscle from either genotype, whereas 35 mM glucose inhibited insulin-stimulated (20 nM) 3-O-methylglucose transport by 65% in wild-type and 99% in GLUT4-null mice. We utilized the 2-N-4-1-(1-azi-2,2,2-t r i f l u o r o e t h y l ) b e n z o y l - 1, 3 - b i s (D - m a n n o s e - 4 - y l o x y ) - 2 - p ro p y lamine (ATB-BMPA) exofacial photolabel to determine if increased cell-surface GLUT1 or GLUT4 content accounted for insulin-stimulated glucose transport in GLUT4-null muscle. In wild-type soleus muscle, cell-surface GLUT4 content was increased by 2.8-fold under insulin-stimulated conditions and this increase corresponded to the increase in 2-deoxyglucose uptake. No detectable cell-surface GLUT4 was observed in soleus muscle from female GLUT4-null mice under either basal or insulin-stimulated conditions. Basal cell-surface GLUT1 content was similar between wild-type and GLUT4-null mice, with no further increase noted in either genotype with insulin exposure. Neither GLUT3 nor GLUT5 appeared to account for insulin-stimulated glucose-transport activity in wild-type or GLUT4-null muscle. In conclusion, insulin-stimulated glucose-transport activity in female GLUT4-null soleus muscle is mediated by a facilitative transport process that is glucose- and cytochalasin B-inhibitable, but which is not labelled strongly by ATB-BMPA.


1999 ◽  
Vol 342 (2) ◽  
pp. 321 ◽  
Author(s):  
Jeffrey W. RYDER ◽  
Yuichi KAWANO ◽  
Alexander V. CHIBALIN ◽  
Jorge RINCÓN ◽  
Tsu-Shuen TSAO ◽  
...  

1995 ◽  
Vol 14 (2) ◽  
pp. 263-275 ◽  
Author(s):  
D M Thomas ◽  
S D Rogers ◽  
M W Sleeman ◽  
G M Pasquini ◽  
F R Bringhurst ◽  
...  

ABSTRACT This study characterizes the actions of insulin and parathyroid hormone (PTH) on the glucose transport system in the rat osteogenic sarcoma cell line UMR 106–01, which expresses a number of features of the osteoblast phenotype. Using [1,2-3H]2-deoxyglucose (2-DOG) as a label, UMR 106–01 cells were shown to possess a glucose transport system which was enhanced by insulin. In contrast, PTH influenced glucose transport in a biphasic manner with a stimulatory effect at 1 h and a more potent inhibitory effect at 16 h on basal and insulin-stimulated 2-DOG transport. To explore the mechanism of PTH action, a direct agonist of cAMP-dependent protein kinase (PKA) was tested. 8-Bromo-cAMP had no acute stimulatory effect but inhibited basal and insulin-stimulated 2-DOG transport at 16 h. This result suggested that the prolonged, but not the acute, effect of PTH was mediated by the generation of cAMP. Further studies with the cell line UMR 4–7, a UMR 106–01 clone stably transfected with an inducible mutant inactive regulatory subunit of PKA, confirmed that the inhibitory but not the stimulatory effect of PTH was mediated by the PKA pathway. Northern blot data indicated that the prolonged inhibitory effects of PTH and 8-bromo-cAMP on glucose transport were likely to be mediated in part by reduction in the levels of GLUT1 (HepG2/brain glucose transporter) mRNA.


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