Effect of fasting on tubular phosphorus reabsorption

Beck, Nama; Webster, S. K.; Reineck, H. J.

doi:10.1152/ajprenal.1979.237.3.f241

Cited by 12 publications

(17 citation statements)

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“…In tubules isolated from LPD rats, the GNG rate was found to be decreased (49). It is tempting to speculate that lack of a response to PTH (or to DBcAMP) in animals fed LPD (7,8) may be due to suppressed GNG (49), and consequently to insufficient generation of cytoplasmic NAD+ needed to inhibit BBM uptake to Pi, in spite of an adequate supply of intracellular or extracellular cAMP. Such an explanation seems to be in agreement with our recent finding (39) which showed that infusion of PTH to rats maintained on NPD caused both phosphaturia and an increase in NAD+/NADH ratio, whereas in rats on LPD, both UpiV and NAD+/NADH ratio failed to increase in the response to PTH (39).…”

Section: Discussionmentioning

confidence: 99%

“…However, cAMP added directly to the BBM vesicles in vivo had no effect on the BBM uptake of Pi (1, Kempson and Dousa, unpublished observations). Prominent changes in the rate of BBM uptake of Pi caused by variation of the dietary Pi intake (1,2) or by starvation (5), seem to occur independently of the regulatory influence of cAMP (1,6,7). Thus, although cAMP may indeed play a role in the actions of some phosphaturic hormones (e.g., PTH, calcitonin) (8), the intracellular factors which regulate the rate of Pi transport across BBM of proximal tubules in response to various pathophysiologic states remain to be identified (8).…”

Section: Introductionmentioning

confidence: 99%

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Possible role of nicotinamide adenine dinucleotide as an intracellular regulator of renal transport of phosphate in the rat.

Kempson¹,

Colón‐Otero²,

Ou³

et al. 1981

J. Clin. Invest.

120

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A B S T R A C T In these experiments we investigated whether NAD could serve as an intracellular modulator of the brush border membrane (BBM) transport of inorganic phosphate (Pi). NAD, both oxidized (NAD+) and reduced (NADH) form, inhibited the Na+-dependent uptake of 32Pi in the concentration range of 10-300 zM NAD when added in vitro to BBM vesicles isolated from rat kidney cortex, but did not inhibit BBM uptake of D-[3H]glucose or BBM uptake of 22Na+. Neither nicotinamide (NiAm) nor adenosine alone influenced BBM uptake of 32Pi. NAD had a similar relative effect (percent inhibition) in BBM from rats stabilized on low Pi diet (0.07% Pi), high Pi diet (1.2% Pi), or normal Pi diet (0.7% Pi).Subsequently, we examined the renal effects of changing the tissue NAD level in vivo. Rats stabilized on low Pi diet were injected intraperitoneally with NiAm (0.25-1.0 g/kg body wt); urinary excretions of Pi (UpV), of fluid, and of other solutes were measured before and after NiAm injection, then renal cortical tissue nucleotide content was determined, and a BBM fraction was isolated for transport measurements. In BBM from NiAm-treated rats, the Na+-dependent uptake of 32Pi was decreased, but BBM uptake of D-[3H]glucose and BBM uptake of22Na+ were not changed. NiAm 29 December 1980. mum change, 290%), a lesser increase in NADH (maximum change, +45%), but no change in the content of ATP or cyclic AMP in the renal cortex. Na+-dependent BBM uptake of 32Pi was inversely correlated with NAD+ content in renal cortex (r = -0.77+0.1; P < 0.001) arid with UpiV (r = -0.67+0.13; P < 0.01). NAD+ in renal cortex was positively correlated with UpjV (r = 0.88±0.05; P < 0.001). Injection of NiAm elicited a marked increase in Up1V, but no change in excretions of creatinine or K+, or in urine flow; excretion of Na+ and Ca declined. NiAm injection caused similar renal responses, in normal and in thyroparathyroidectomized rats, as well as in rats on normal Pi diet and low Pi diet.We conclude that NAD can serve as an intracellular modulator (inhibitor) of Na+-dependent transport of Pi across the renal luminal BBM and across the proximal tubular wall by its direct interaction with BBM. We propose that at least some hormonal and/or metabolic stimuli elicit phosphaturia by increasing NAD+ in cytoplasm of proximal tubular cells. INTRODUCTIONA Na+-dependent Pi uptake by the luminal brush border membrane (BBM) and its regulation by various hormonal and metabolic stimuli (1-3) are initial and perhaps quantitatively determining cellular steps in proximal tubular reabsorption of phosphate (Pi). Parathyroid hormone (PTH) or vitamin D (1, 3) has been reported to decrease BBM uptake ofPi, whereas growth hormone reportedly has an opposite effect (4). In phosphaturia associated with starvation (5) or a high Pi diet (2), the capacity of the BBM to transport Pi is diminished; feeding with a diet selectively deficient in Pi, however, leads to a marked increase in BBM uptake of Pi (1)(2)(3)5), which is apparently independent of the J. Clin. (5, 16). HPD ...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Possible role of nicotinamide adenine dinucleotide as an intracellular regulator of renal transport of phosphate in the rat.

Kempson¹,

Colón‐Otero²,

Ou³

et al. 1981

J. Clin. Invest.

120

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“…It has become apparent as a result of several phy siological studies that starvation has an effect on calcium metabolism \ Kcilu and Foster, 1976;Ascii, 1978;Beck et al, 1979;Pak and Galosy, 1979;Shires et al, 1980;Asch and Ascii, 1981]. However, there is no study on the effects of starvation on the ultrastructure of the pa rathyroid gland related to calcium and phosphorus metabolism.…”

Section: Introductionmentioning

confidence: 99%

Effects of Starvation on the Ultrastructure of the Mouse Parathyroid Gland

Isono¹,

Shoumura²,

Ishizaki³

et al. 1985

Cells Tissues Organs

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Ultrastructural changes of the parathyroid glands of starved mice were examined. The parathyroid glands of the starved mice showed a decrease in the volume of Golgi complexes and storage granules and an increase in the volume of lipid droplets, and contained more heterogeneously dense bodies and multivesicular bodies compared with that of the control mice. In addition, the volume of mitochondria, cisternae of granular endoplasmic reticulum and secretory granules and the number of prosecretory granules appeared to be decreased compared to those of the control mice. Myelin-like structures were observed in the parathyroid glands of the starved mice. The results of our study provide support for the hypothesis that starvation exerts an inhibitory influence not only on the synthesis but also on release of parathyroid hormone.

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“…Physiological studies have shown that starvation had an effect on calcium metabolism (Kalu and Foster, 1976;Asch, 1978;Beck et al, 1979;Pak and Galosy, 1979;Shires et al, 1980;Asch and Asch, 1981). Recent morphological reports have suggested the changes of the parathyroid glands in starved mice (Isono et al , 1985) and starved golden hamsters .…”

Section: Starvationmentioning

confidence: 99%