Transcellular transport of calcium and inorganic phosphate in the small intestinal epithelium

Murer, Heini; Hildmann, Bruno

doi:10.1152/ajpgi.1981.240.6.g409

Cited by 40 publications

(30 citation statements)

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“…Arsenate is a known inhibitor of P i transport (Murer and Hildmann, 1981). In the present study, mucosally-applied arsenate inhibited the J MS of P i such that the active component of P i absorption was abolished (Table 3).…”

Section: Discussionsupporting

confidence: 56%

Sodium-Phosphate Symport by Aplysia Californica Gut

2002

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Section: Discussionsupporting

confidence: 56%

Sodium-Phosphate Symport by Aplysia Californica Gut

2002

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“…UF Ca will increase to such an extent that the elevated UF Ca exceeds the increase in fr Ca , leading to an absolute increase in U Ca (38,39). In many patients, the excess PTH stimulates an increase in 1,25(OH) 2 D 3 (40), resulting in an increase in ␣ Ca and the product D Ca ϫ ␣ Ca (41,42 (43)(44)(45)(46)(47).…”

Section: Normal Individualsmentioning

confidence: 99%

Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content

Bushinsky

2010

Clinical Journal of the American Society of Nephrology

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Calcium (Ca) balance is the net of Ca intake and output from the body over a period of time. The concept of Ca balance does not consider the redistribution of Ca that often occurs in patients with chronic kidney disease (CKD), especially those who are on dialysis, which is often in the form of soft tissue and/or vascular calcification. In this article, we consider movement of Ca with respect to the extracellular fluid (ECF) and develop a mathematical formulation for Ca homeostasis with respect to the ECF that includes input and output from the diet, the bone, the kidney, and dialysis. We consider calcium homeostasis in healthy individuals and in patients with excess parathyroid hormone, excess 1,25-dihydroxyvitamin D 3 , and metabolic acidosis; patients who have CKD and are not on dialysis; and, finally, patients who have CKD and are on dialysis. On the basis of a number of assumptions, dialysis patients with a daily intake of >37.5 mmol of elemental Ca (1.5 g) have movement of Ca into the ECF even without supplemental activated vitamin D. Addition of activated vitamin D, which increases intestinal Ca absorption and can increase resorption of Ca from bone, leads to the movement of Ca into the ECF at virtually all levels of intake; however, there are numerous unanswered questions regarding Ca homeostasis in patients with CKD, including how much of the Ca, administered as a phosphate binder, is absorbed and what is the fate of this absorbed Ca. Until these pressing questions are answered with well-designed experiments, we do not know whether we are doing more harm than good for our dialysis patients by administering additional Ca as a phosphate binder, especially when they also receive activated vitamin D.

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“…The transport of phosphate across the small intestine of suckling and adult animals occurs by an active process (1)(2)(3)(4)(5). Jejunal phosphate transport take place against an electrochemical gradient and is inhibited by arsenate (1)(2)(3)(4)(5)(6)(7)(8).…”

mentioning

confidence: 99%

“…Jejunal phosphate transport take place against an electrochemical gradient and is inhibited by arsenate (1)(2)(3)(4)(5)(6)(7)(8). The uptake of phosphate at the brush border membrane consists of two components: a saturable, electroneutral sodium dependent component and an unsaturable, sodium-independent component (1, 2).…”

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confidence: 99%

“…The uptake of phosphate at the brush border membrane consists of two components: a saturable, electroneutral sodium dependent component and an unsaturable, sodium-independent component (1, 2). The energy driving the sodium-dependent entry of phosphate into the cell is provided by an extracellular to intracellular Na+ gradient maintained by the Na+-K+-ATPase at the basolateral membrane (5). Both sodium-dependent and -independent brush border phosphate uptake are higher in suckling rats compared to adult rats (6).…”

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confidence: 99%

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Phosphate Transport hy Intestinal Endoplasmic Reticulum during Maturation

Arab

1988

Pediatr Res

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ABSTRAm. The transport of phosphate into jejunal endoplasmic reticulum vesicles isolated from suckling and adolescent rats was investigated using a rapid filtration technique. Intestinal endoplasmic reticulum from both ages were enriched with NADPH cytochrome-C-reductase whereas other markers for brush border, basolateral, mitochondrial, and Golgi apparatus were impoverished. Phosphate uptake represented an energy-dependent process as evident by more than 80% decrease in uptake values at 0" C compared to 25" C. Phosphate uptake was ATP dependent in both age groups, however, mean uptake values were significantly greater in suckling rats compared to adolescent rats. pH optimum for uptake was 7.2. p-Chloromercuribenzoate at 100 pM concentration inhibited phosphate uptake by more than 90%. Initial rate of phosphate uptake was linear up to 45 s. Kinetics of phosphate uptake at 30 s showed a K, of 0.7 + 0.1 and 0.15 2 0.1 suckling and adolescent rats, respectively. V,., was 1.5 + 0.5 and 0.14 f 0.01 nmol/mg protein/30 s for both suckling and adolescent rats, respectively. Herein we provide evidence for the first time for the presence of a phosphate carrier in intestinal endoplasmic reticulum of rats. Endoplasmic reticulum of phosphate uptake was significantly greater in suckling rats compared to adolescent rats. This increase in uptake is due to a greater number and activity of phosphate carriers in suckling rats. (Pediatr Res 23: 612-615, 1988)The transport of phosphate across the small intestine of suckling and adult animals occurs by an active process (1-5). Jejunal phosphate transport take place against an electrochemical gradient and is inhibited by arsenate (1-8). The uptake of phosphate at the brush border membrane consists of two components: a saturable, electroneutral sodium dependent component and an unsaturable, sodium-independent component (1, 2). The energy driving the sodium-dependent entry of phosphate into the cell is provided by an extracellular to intracellular Na+ gradient maintained by the Na+-K+-ATPase at the basolateral membrane (5). Both sodium-dependent and -independent brush border phosphate uptake are higher in suckling rats compared to adult rats (6). Phosphate exit at the basolateral membrane of the enterocyte occurs by a camer-mediated process that is sodium dependent, electroneutral with stoichiometry of 2 Na:l phosphate at pH 7.4 (7). The transcellular movement of phosphate is unknown. Recently, we described an important role for the endoplasmic reticulum in transcellular calcium transport (8). This process is ATP dependent and exhibits characteristic devel- opmental patterns (8). Our study was designed to investigate the role of intestinal endoplasmic reticulum in phosphate transport during maturation in the rat. We used a millipore filtration system to study phosphate uptake by intestinal microsomes. EXPERIMENTAL PROCEDURES Isolation of intestinal endoplasmic reticulum vesicles.The jejunum of two adolescent rats (42 + 2 days) of 12 suckling rats (14 + 1 day) were used to prepare the en...

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Transcellular transport of calcium and inorganic phosphate in the small intestinal epithelium

Cited by 40 publications

References 0 publications

Sodium-Phosphate Symport by Aplysia Californica Gut

Sodium-Phosphate Symport by Aplysia Californica Gut

Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content

Phosphate Transport hy Intestinal Endoplasmic Reticulum during Maturation

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