scholarly journals Na+-dependent transport system for taurocholate in rat small intestine; Its localization in the terminal ileum and variation by fasting.

1990 ◽  
Vol 54 (3) ◽  
pp. 685-689 ◽  
Author(s):  
Masaru KITAGAWA ◽  
Kimikazu IWAMI ◽  
Fumio IBUKI
Keyword(s):  
Small Intestine ◽  
Transport System ◽  
Terminal Ileum ◽  
Rat Small Intestine ◽  
Dependent Transport

Functional characterization of PCFT/HCP1 as the molecular entity of the carrier-mediated intestinal folate transport system in the rat model

2008 ◽  
Vol 294 (3) ◽  
pp. G660-G668 ◽  
Author(s):  
Katsuhisa Inoue ◽  
Yasuhiro Nakai ◽  
Sayaka Ueda ◽  
Shunsuke Kamigaso ◽  
Kin-ya Ohta ◽  
...  
Keyword(s):  
Small Intestine ◽  
Transport System ◽  
Functional Characterization ◽  
Cellular Membrane ◽  
Molecular Entity ◽  
Xenopus Laevis Oocytes ◽  
Rat Small Intestine ◽  
Distribution Profile ◽  
Folate Transport

Proton-coupled folate transporter/heme carrier protein 1 (PCFT/HCP1) has recently been identified as a transporter that mediates the translocation of folates across the cellular membrane by a proton-coupled mechanism and suggested to be the possible molecular entity of the carrier-mediated intestinal folate transport system. To further clarify its role in intestinal folate transport, we examined the functional characteristics of rat PCFT/HCP1 (rPCFT/HCP1) expressed in Xenopus laevis oocytes and compared with those of the carrier-mediated folate transport system in the rat small intestine evaluated by using the everted tissue sacs. rPCFT/HCP1 was demonstrated to transport folate and methotrexate more efficiently at lower acidic pH and, as evaluated at pH 5.5, with smaller Michaelis constant ( Km) for the former (2.4 μM) than for the latter (5.7 μM), indicating its characteristic as a proton-coupled folate transporter that favors folate than methotrexate as substrate. rPCFT/HCP1-mediated folate transport was found to be inhibited by several but limited anionic compounds, such as sulfobromophthalein and sulfasalazine. All these characteristics of rPCFT/HCP1 were in agreement with those of carrier-mediated intestinal folate transport system, of which the Km values were 1.2 and 5.8 μM for folate and methotrexate, respectively, in the rat small intestine. Furthermore, the distribution profile of the folate transport system activity along the intestinal tract was in agreement with that of rPCFT/HCP1 mRNA. This study is the first to clone rPCFT/HCP1, and we successfully provided several lines of evidence that indicate its role as the molecular entity of the intestinal folate transport system.

scholarly journals Phosphate transport into brush-border membrane vesicles isolated from rat small intestine

1976 ◽  
Vol 160 (3) ◽  
pp. 467-474 ◽  
Author(s):  
W Berner ◽  
R Kinne ◽  
H Murer
Keyword(s):  
Small Intestine ◽  
Transport System ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Electrical Potential ◽  
Membrane Vesicles ◽  
Sodium Concentration ◽  
Phosphate Transport ◽  
Brush Border Membrane Vesicles ◽  
Rat Small Intestine

Uptake of Pi into brush-border membrane vesicles isolated from rat small intestine was investigated by a rapid filtration technique. The following results were obtained. 1. At pH 7.4 in the presence of a NaCl gradient across the membrane (sodium concentration in the medium higher than sodium concentration in the vesicles), phosphate was taken up by a saturable transport system, which was competitively inhibited by arsenate. Phosphate entered the same osmotically reactive space as D-glucose, which indicates that transport into the vesicles rather than binding to the membranes was determined. 2. The amount of phosphate taken up initially was increased about fourfold by lowering the pH from 7.4 to 6.0.3. When Na+ was replaced by K+, Rb+ or Cs+, the initial rate of uptake decreased at pH 7.4 but was not altered at pH 6.0.4. Experiments with different anions (SCN-,Cl-, SO42-) and with ionophores (valinomycin, monactin) showed that at pH 7.4 phosphate transport in the presence of a Na+ gradient is almost independent of the electrical potential across the vesicle membrane, whereas at pH 6.0 phosphate transport involves the transfer of negative charge. It is concluded that intestinal brush-border membranes contain a Na+/phosphate co-transport system, which catalyses under physiological conditions an electroneutral entry of Pi and Na+ into the intestinal epithelial cell. In contrast with the kidney, probably univalent phosphate and one Na+ ion instead of bivalent phosphate and two Na+ ions are transported together.

scholarly journals The effect of starvation on the control of phosphofructokinase activity in the epithelial cells of the rat small intestine

1983 ◽  
Vol 210 (1) ◽  
pp. 129-135 ◽  
Author(s):  
A Jamal ◽  
G L Kellett
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Terminal Ileum ◽  
Specific Activity ◽  
Utilization Rate ◽  
Proximal Jejunum ◽  
Rat Small Intestine ◽  
Humoral Factors ◽  
Specific Activities ◽  
Regulatory Properties

1. The effect of depriving rats of food for 48 h on the specific activity of phosphofructokinase in the epithelial cells of the small intestine and on the regulatory properties of the enzyme displayed in crude (particle-free) mucosal extracts was studied. 2. The specific activity of phosphofructokinase, measured under optimal conditions at pH8, in the mucosa of fed rats showed a negative aboral gradient along the intestine, decreasing from 15.2 +/- 1.2 units (mumol/min)/g wet wt. in the proximal jejunum to 4.6 +/- 1.2 units/g wet wt. in the terminal ileum. 3. After starvation, the gradient was diminished, but not abolished; the diminution in gradient was due almost exclusively to a decrease in the specific activity of phosphofructokinase in the proximal jejunum by about 30%, there being no change in the terminal ileum. 4. In fed rats, the susceptibility of phosphofructokinase to inhibition by ATP, when assayed in crude mucosal extracts under suboptimal conditions, was independent of length along the small intestine; the ratio of the activity observed at pH 7.0 in the presence of 0.5 mM-fructose 6-phosphate and 2.5 mM-ATP to the optimal activity at pH 8, v0.5/V, was 0.36 +/- 0.05 in the proximal jejunum and 0.42 +/- 0.07 in the terminal ileum. 5. After starvation, the susceptibility of phosphofructokinase to inhibition by ATP was increased and was again found to be independent of length along the small intestine: after starvation, v0.5/V was 0.19 +/- 0.04 and 0.20 +/- 0.07 for the proximal jejunum and the terminal ileum respectively. 6. Re-feeding of previously starved rats on a high-carbohydrate diet overnight for 16 h restored both the specific activities of phosphofructokinase and its susceptibility to inhibition by ATP to normal values for fed rats. 7. The data support the idea that the specific activities and the regulatory properties of phosphofructokinase in the epithelial cells of rat small intestine are mediated by distinct humoral factors. 8. The changes in glucose utilization rate of the jejunum when rats are starved can in principle be accounted for by a combination of changes in the specific activity and in the regulatory properties of mucosal phosphofructokinase.

Glucose and sorbose absorption at various levels of rat small intestine

1961 ◽  
Vol 200 (2) ◽  
pp. 301-304 ◽  
Author(s):  
R. David Baker ◽  
Gordon W. Searle ◽  
Arthur S. Nunn
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Terminal Ileum ◽  
Glucose Absorption ◽  
Lower Half ◽  
Rat Small Intestine ◽  
Glucose Transfer ◽  
Constant Rate ◽  
Fluoride Poisoning

The passage of glucose and sorbose across the wall at various levels of rat small intestine has been studied in vitro. ‘Uphill’ glucose transport was demonstrated in the jejunum and upper half of the ileum but could not be seen in the terminal quarter of small intestine. Aerobically, in the mid-jejunum glucose absorption from the mucosal solution was about 5.5 times as rapid as in the terminal ileum; the aboral decline in absorptive activity, however, occurred only in the lower half of the small intestine; the upper half absorbed glucose at a nearly constant rate throughout. No aboral decline for rate of glucose transfer into the serosal solution was noticed in the upper three-quarters of small intestine, but in the lower quarter the drop was precipitous. The effects of hypoxia and fluoride poisoning, respectively, on glucose movements were much more severe in the upper than in the lower portions of small intestine. Fluoride (48 mm) completely abolished the absorptive activity gradient for glucose along the small intestine. Sorbose movements were quite similar in rate to the fluoride-inhibited glucose movements.

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