Effects Of Phosphate Depletion Research Articles

Shifts in regional production as a driver of future global ocean production stoichiometry

Using a global ocean biogeochemistry model, we examined three drivers of global ocean production C:N:P ratio: flexible phytoplankton stoichiometry, phytoplankton community composition, and regional production shifts. For a middle-of-the-road warming scenario (SSP2), the model predicts a substantial increase in the global export C:P ratio from 113:1 to 119:1 by the year 2100. The most important physiological driver of this stoichiometric change is the effect of the worldwide warming on cyanobacteria, followed by the effect of phosphate depletion on eukaryotes in the Southern Ocean. Also, there is a modest global shift in the phytoplankton community in favor of cyanobacteria at the expense of eukaryotes with a minimal effect on the global production stoichiometry. We find that shifts in the regional production, even in the absence of any change in phytoplankton stoichiometry or taxonomy, can change the global production C:N:P ratio. For example, enhancing the production in the polar waters, which typically have low C:N:P ratios, will have the effect of lowering the global ratio. In our model, the retreat of Antarctic sea ice has this very effect but is offset by production changes downstream and elsewhere. This study thus provides an understanding of how regional production changes can affect the global production C:N:P ratio. However, the current literature indicates substantial uncertainty in the future projections of regional production changes, so it is unclear at this time what their net effect is on the global production C:N:P ratio. Finally, our model predicts that the overall increase in the carbon content of organic matter due to flexible C:N:P ratio helps to stabilize carbon export in the face of reduced nutrient export (i.e. the decrease in C export is ~30% smaller than expected from the decrease in P export by 2100) but has a minimal effect on atmospheric CO2 uptake (~1%).

Sugar-regulated control of α-tubulin in maize cell suspension culture

The data reported here shows that α-tubulin, the subunit of microtubulin in the cytoskeleton, is regulated by sugars. A 48-h sugar-depletion treatment in BMS maize cell suspension culture medium led to a marked reduction in the levels of α-tubulin mRNA and protein. This response was reversible; the addition of metabolizable sugars led to a rapid increase in the levels of the α-tubulin transcript. Levels of α-tubulin protein also increased, albeit gradually. Surprisingly, there was little or no effect of phosphate depletion and phosphate addition on α-tubulin expression. Furthermore, the data show that sugars modulate a co-regulation of α-tubulin and cell-wall invertase. We propose that microtubules might be a major component of a sugar-signaling pathway that is regulated by, among other factors, cellular carbon metabolism.

Phosphate depletion diminishes Mg2+ uptake in mouse distal convoluted tubule cells

Hypophosphatemia caused by phosphate depletion is associated with renal magnesium wasting. The cellular mechanisms of phosphate depletion were investigated in an immortalized mouse distal convoluted tubule (MDCT) cell line. Intracellular free Mg2+ concentration. [Mg2+]i was determined by microfluorescence. Mg2+ transport was assessed as a function of change in [Mg2+]i with time following placement of Mg(2+)-depleted cells into a buffer containing 1.5 mM magnesium. The uptake rate of Mg2+ into Mg(2+)-depleted cells cultured in normal phosphate, 1.0 mM, was 175 +/- 21 nM/second. Depletion of phosphate in the culture media was associated with a significant decrease in Mg2+ uptake, which was dependent on the degree of phosphate depletion and on the time cultured in phosphate-deficient media. Cells cultured for 16 hours in 0.3 mM and 0 mM phosphate possessed Mg2+ uptake rates of 105 +/- 18 nM/second and 15 +/- 12 nM/second, respectively. Diminished Mg2+ uptake was rapidly induced following placement in low phosphate and was fully reversed following readdition of phosphate to the culture media. The effects of phosphate depletion on Mg2+ uptake was post-translational in nature as fully up-regulated MDCT cells with maximal Mg2+ uptake was associated with a rapid decrease (within 30 min) in Mg2+ transport when placed in phosphate-deficient media. Although Mg2+ uptake is altered by the transmembrane voltage, diminished Mg2+ uptake associated with phosphate depletion was not dependent on changes in membrane voltage. Further, it was not associated with a sustained increase in intracellular Ca2+ concentration. Chlorothiazide, probably through hyperpolarization of the plasma membrane, stimulates Mg2+ uptake in normal. 283 +/- 23 nM/second, and phosphate-depleted cells, 203 +/- 29 nM/second, but failed to entirely correct the defective transport. These studies demonstrate that magnesium wasting associated with hypophosphatemia and phosphate depletion is due, in part, to diminished Mg2+ transport in the distal convoluted tubule. The evidence is that the actions of phosphate deficiency are through alterations of Mg2+ transport across the luminal membrane of the distal convoluted tubule cell.

Management of Diabetic Ketoacidosis

Diabetic ketoacidosis is an all too frequent and sometimes preventable complication of Type I diabetes mellitus, responsible for significant morbidity and mortality within the diabetic population. Precipitating diseases account for the majority of deaths occurring in patients admitted in diabetic ketoacidosis, but some deaths are still attributable to ketoacidosis alone, despite recent advances in therapy and management. Recognition of the ketoacidotic state is paramount to optimal therapy, and often hinges on the diagnostic acumen of the physician. Since 20 to 30% of patients presenting in diabetic ketoacidosis do so as the initial manifestation of their previously undiagnosed disease, physicians must maintain a high level of suspicion for this condition. Understanding the pathogenetic mechanisms leading to and prevailing in diabetic ketoacidosis will allow physicians to intervene in a rational manner, approaching therapy with specific end-points in mind: (a) restoration of optimal volume status; (b) reversal of acidosis; (c) reduction of serum glucose levels; (d) replacement of specific electrolytes in a timely manner; (c) institution of appropriate therapy for any precipitating cause; and, (f) careful monitoring of the patient's biochemical, physical and mental parameters to allow adjustment in therapy as necessary. The mainstay of treatment for diabetic ketoacidosis is appropriate fluid and insulin therapy. Low-dose intravenous infusion is now the accepted mode of insulin delivery for patients with this condition. Potassium replacement is almost always necessary, often requiring massive amounts of this ion due to the total body depletion seen with the development of ketoacidosis. Controversy still surrounds routine use of phosphate in diabetic ketoacidosis but replacement may be needed if serum levels fall toward the lower limits of normal values, to avoid the potential adverse effects of phosphate depletion. Administration of bicarbonate is also controversial and should be reserved for patients whose pH is less than 7.0 to 7.1 and then it should be added to intravenous fluids, not given as an intravenous bolus. Efforts toward preventing diabetic ketoacidosis should be of prime importance to physician and patient alike. Preventive measures should include patient education about diabetes mellitus, precipitating factors of diabetic ketoacidosis, signs and symptoms of early metabolic decompensation, rational insulin therapy during minor illness and appropriate timing of physician contact to help avoid this serious and sometimes fatal complication of diabetes mellitus.

Consequences of phosphate imbalance.

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.

Effect of phosphate depletion on blood pressure and vascular reactivity to norepinephrine and angiotensin II in the rat.

Phosphate depletion (PD) adversely affects myocardial function but its influence on blood pressure is not well elucidated. In this study we evaluated whether PD influences blood pressure and/or affects its hormonal regulation or the peripheral vascular response to pressor agonists. Mean arterial pressure (MAP) in PD rats was lower than in normal animals, whereas heart rate was not significantly different between the two groups. Cardiac index (CI) in PD rats was lower and systemic vascular resistance (SVR) was higher than in controls. Plasma norepinephrine (NE) in the resting state and during the stress of immobilization was significantly greater in PD rats than in controls. Base-line plasma renin activity was also significantly higher in PD rats and increased similarly in the two groups of rats after administration of isoproterenol. Bolus injections of NE or angiotensin II produced a smaller rise in MAP in PD rats than in controls. Reduced responsiveness to NE was also demonstrated in isolated hind-limb preparation from PD rats. When NE was infused to achieve a rise in MAP of 30 mmHg, the dose required in PD was higher than in controls. Treatment with indomethacin did not affect the response in MAP to NE. The content and affinity of both alpha- and beta-receptors in PD hearts were not different from those of control hearts. The contents of PiATP, and AMP in the mesenteric vessels of PD rats were significantly lower than in control animals. These data show that PD leads to reductions in MAP, arteriolar response to pressor agents, and CI with appropriate compensatory rise in NE but with inadequate compensatory increase in SVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired energy metabolism in skeletal muscle during phosphate depletion

AbstractImpaired energy metabolism in skeletal muscle during phosphate depletion. The effects of phosphate depletion (PD) of 4, 8, and 12 weeks on skeletal muscle energy metabolism were studied in rats fed a phosphate deficiency diet and compared with rats pairfed with a normal phosphate diet. Skeletal muscle biopsy specimens were examined for energy production, transport, and utilization. The results show that already by 4 weeks of PD, the concentration of inorganic phosphorus of the skeletal muscle was significantly reduced and remained low thereafter. There was significant (P < 0.01) and direct correlation between the cellular inorganic phosphorus and that of serum phosphorus. Adenine nucleotides, ATP, ADP, AMP, and creatine phosphate levels did not change. Mitochondrial respiration and oxidative phosphorylation were impaired by PD. Total cellular mitochondrial and myofibrillar creatine phosphokinase activities were significantly reduced at 4 weeks of PD and fell further at 8 and 12 weeks. There was a significant (P < 0.01) and direct correlation between the activity of total extractable creatine phosphokinase and both serum and cellular levels of inorganic phosphorus. These data show that chronic PD is associated with a decrease in energy production, transfer, and utilization by skeletal muscle and provides information on the molecular events responsible for the myopathy of PD.Alteration du metabolisme energetique dans le muscle squellettique pendant la depletion phosphate. Les effets d'une déplétion phosphatée (PD) pendant 4, 8, et 12 semaines sur le métabolisme énergétique du muscle squelettique ont été étudiés chez des rats recevant un régime déficient en phosphate et comparés avec des rats nourris de façon appariée avec un régime normal en phosphate. Des spécimens biopsies de muscles squelettiques ont été examinées pour la production, le transport, et l'utilisation d'énergie. Les résultats indiquent que déjà à 4 semaines de PD, la concentration de phosphore inorganique dans le muscle squelettique était significativement réduite et restait basse ensuite. Il y avait une corrélation significative (P < 0.01) et directe entre le phosphore cellulaire inorganique et le phosphore sérique. Les niveaux d'adénine nucléotides, ATP, ADP, AMP, et de créatine phosphate n'ont pas changé. La respiration mitochondriale et la phosphorylation oxydative étaient altérées par la PD. Les activités créatine-phospho-kinase cellulaire totale, mitochondriale et myofibrillaire étaient significativement réduites à 4 semaines de PD et s'abaissaient encore à 8 et 12 semaines. Il y avait une corrélation significative (P < 0.01) et directe entre l'activité de la créatine-phospho-kinase totale extractible et à la fois les concentrations de phosphore inorganique sériques et cellulaires. Ces données indiquent que la PD chronique est associée à une diminution de la production, du transfert et de l'utilisation d'énergie par le muscle squelettique, et elles apportent une information sur les anomalies moléculàires responsables de la myopathie de la PD.

Impaired energy metabolism in rat myocardium during phosphate depletion.

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

Effects of phosphate depletion on the myocardium.

Indirect evidence suggests that cardiac function may be affected by phosphate depletion (PD). Coburn and Massry (l) found that glomerular filtration rate is reduced during phosphate depletion and it returned to normal with phosphate repletion. They suggested that this phenomenon may be related to alteration in cardiac function. O’Connor, Wheeler and Bethune (2) evaluated the effect of PD on cardiac function in seven patients. They found that stroke work was reduced but returned to normal after phosphate administration. Cardiac output, as well as left ventricular stroke volume, were decreased and correlated with the rise in pulmonary artery wedge pressures. The authors showed that with the correction of the hypophosphatemia, left ventricular stroke volume improved and pulmonary artery wedge pressure decreased. Their studies were the first direct demonstration that phosphate depletion may affect cardiac function in man.KeywordsCreatine PhosphateInorganic PhosphorusCreatine PhosphokinasePulmonary Artery Wedge PressureLeft Ventricular Stroke VolumeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Phosphate and acid-base homeostasis.

Both because of its properties as a buffer and its function as a major intracellular anion, phosphate plays a pivotal role in the maintenance of acid-base homeostasis. This review is concerned with the impact of phosphate on three interrelated aspects of acid-base physiology and pathophysiology. These are the role of phosphate as a urinary buffer, its relationship to the formation of urinary carbon dioxide tension, and the effects of phosphate depletion on urinary acidification.KeywordsRenal Tubular AcidosisDistal NephronUrinary AcidificationDistal Renal Tubular AcidosisPhosphate DepletionThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Effects of phosphate depletion on acid-base status in dogs

Hyperchloremic acidosis may occur in patients with severe hypophosphatemia, including some with hyperparathyroidism. In experimental models of phosphate depletion, metabolic acidosis has not been a consistent feature. In some studies, arterial pH values have been normal, but have been associated with high rates of urinary bicarbonate loss. In other studies, metabolic acidosis has been observed associated with a decreased capacity for renal bicarbonate reabsorption. The present study was designed to examine the effects of both phosphate depletion upon systemic acid-base status in dogs and chronic hypophosphatemia upon renal bicarbonate reabsorption. Studies were performed upon three groups. All received a standard diet markedly diminished in phosphate content. Normal dogs (group I) received a dietary supplement of phosphate (31 m M/day). Group II dogs received no supplemental phosphate. Group III dogs were parathyroidectomized and also received a phosphate-deficient diet. Deprivation of dietary phosphate in groups II and III resulted in severe hypophosphatemia (Serum phosphate = 1.1 mg phosphorus/dl). Renal fractional phosphate reabsorption was increased significantly in both groups. Despite phosphate deprivation for up to 14 wk, arterial pH and bicarbonate values remained normal. Values for fasting urine pH and bicarbonate excretion were similar in the three groups. Renal bicarbonate conservation was normal in groups II and III as observed under fasting conditions. During bicarbonate infusion studies, patterns of bicarbonate reabsorption/glomerular filtration rate were obtained and maximal rates of renal bicarbonate reabsorption were assessed. To correct for possible differences ascribable to the effects of extracellular fluid volume expansion, the ratio of absolute bicarbonate/absolute sodium reabsorption was also examined. Over a wide range of plasma bicarbonate concentrations, no significant differences in this ratio were observed among the three groups. Maximal rates of renal bicarbonate reabsorption were similar in the three groups. The studies demonstrate that prolonged dietary phosphate deprivation in dogs, while resulting in severe hypophosphatemia, may be associated with the maintenance of normal plasma pH and bicarbonate values. Abnormal rates of urinary bicarbonate loss have not been observed. In the absence of metabolic acidosis, bicarbonate reabsorptive capacity and bicarbonate reabsorptive patterns are normal. The study suggests that other causes for the metabolic acidosis in severe phosphate depletion should be sought.

Effect of phosphate depletion on magnesium homeostasis in rats.

The effects of phosphate depletion on magnesium (Mg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell significantly (P < 0.01) from 10.1+/-0.27 (SE) to 5.0+/-0.54 mg/100 ml within 1 day and continued to fall gradually to a level of 1.2+/-0.21 mg/100 ml by the end of the 8th wk. A significant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46+/-2.7 to 126+/-24 mueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300+/-24 mueq/24 h by the 3rd day and remained high ranging between 150-300 mueq/24 h, thereafter. The magnitude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2+/-0.02 to 0.79+/-0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which became evident by the 3rd wk of phosphate depletion. Mg content of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral content because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 mueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or weight of the animals. Our results indicate that phosphate depletion is associated with (a) magnesuria due to a decrease in the net renal tubular reabsorption of Mg with the main source of the urinary losses being bone Mg; (b) hypomagnesemia secondary to the renal leak of Mg; (c) negative Mg balance; and (d) increase in the intestinal fractional absorption of Mg. The latter was not adequate to compensate for the urinary losses of Mg.

Phosphate depletion and adenine nucleotide metabolism in kidney and liver.

Adenosine triphosphate (ATP) and other adenine nucleotides are the major energy coupling mechanism between the energy-producing and the energy-consuming systems in the cells. In a variety of diseased states, an altered metabolism of adenine nucleotides has been implicated in their pathogenesis. There are a few experimental model systems in which one can alter adenine nucleotide metabolism through a different mechanism and study the role of adenine nucleotides in cell functions as shown in Table 1 (1). Although studies using the first three models have been extensively performed, effects of phosphate depletion on the metabolism of adenosine triphosphate and other phosphate compounds in various organ systems have been studied rather to a lesser extent except in red cells, leukocytes, and platelets, where the relationship between a fall in plasma inorganic phosphate (Pi), a fall in tissue Pi, a decrease in tissue ATP, and some forms of cellular dysfunction have been demonstrated (2). Since a major portion of ATP is synthesized from ADP and Pi by oxidative phosphorylation in mitochondria, a deficiency of Pi will result in an impairment of ATP generation. Thus, various organ dysfunctions described in phosphate depletion have been attributed to a fall in the availability of energy-rich phosphate compounds such as ATP. Nevertheless, data on the changes in levels of adenine nucleotides and Pi in different organ systems are limited.

Renal phosphate transport in the phosphate-depleted dogs.

Renal transport of phosphate is known to be requlated by such factors as filtered load of phosphate(1), parathyroid hormone(2), and extracellular volume(3). The effect of dietary intake of phosphate, however, is less well understood. In order to investigate the effect of phosphate depletion on renal phosphate transport, clearance and micropuncture studies were performed in dogs on low phosphate diet to examine the responses to extracellular volume expansion(VE) and parathyroid hormone(PTH).

Effects of phosphate depletion and parathyroid hormone on renal glucose reabsorption.

ARTICLESEffects of phosphate depletion and parathyroid hormone on renal glucose reabsorptionHR Harter, A Mercado, WE Rutherford, H Rodriguez, E Slatopolsky, and S KlahrHR Harter, A Mercado, WE Rutherford, H Rodriguez, E Slatopolsky, and S KlahrPublished Online:01 Dec 1974https://doi.org/10.1152/ajplegacy.1974.227.6.1422MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe early days of nephrology in ColombiaKidney International, Vol. 69, No. 2The Role of Hemodynamic Factors in the Initiation and Progression of Renal DiseaseJournal of Urology, Vol. 133, No. 3Complications of total parenteral nutritionKidney International, Vol. 27, No. 3Intestinal Phosphate TransportRenal glycosuria in renal homograft recipientsKlinische Wochenschrift, Vol. 62, No. 18Phosphate uptake by superficial and deep nephron brush border membranesPfl�gers Archiv European Journal of Physiology, Vol. 400, No. 4Phosphate transport in the kidney8 July 2005Clinical Spectrum of Phosphate Depletion and Its Effects on Urinary AcidificationMechanisms of Progression of Renal DiseaseHemodynamically mediated glomerular injury and the progressive nature of kidney diseaseKidney International, Vol. 23, No. 4Effects of vitamin D metabolites on protein catabolism of muscle from uremic ratsKidney International, Vol. 23, No. 3Compensatory Renal Hemodynamic Injury: A Final Common Pathway of Residual Nephron DestructionAmerican Journal of Kidney Diseases, Vol. 1, No. 5Parathyroid hormone-independent adaptation of the renal handling of phosphate in response to renal mass reductionKidney International, Vol. 21, No. 3Parathyroid HormoneParathyroid hormone inhibition of phosphate transport in renal brush border vesicles from phosphate-depleted dogsBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 645, No. 2Studies on the role of the liver and splanchnic tissues in the production of carbohydrate intolerance in uremiaMetabolism, Vol. 30, No. 7Renal handling of calcium and phosphateKlinische Wochenschrift, Vol. 58, No. 19The Effects of Parathyroid Hormone on Renal Phosphate HandlingTubular Adaptation to the Supply and Requirement of PhosphateReversal of hyperparathyroidism in response to dietary phosphorus restriction in the uremic dogKidney International, Vol. 15, No. 1Renal response to phosphorus deprivation in the isolated rat kidneyKidney International, Vol. 13, No. 2Regulation of the Tubular Transport of Phosphate in the Rat: Role of Parathyroid Hormone and 1,25-Dihydroxyvitamin D3Urinary Phosphate and Cyclic AMP in PseudohypoparathyroidismPhosphate Depletion and Adenine Nucleotide Metabolism in Kidney and LiverImpaired distal nephron acidification in chronically phosphate depleted ratsPfl�gers Archiv European Journal of Physiology, Vol. 377, No. 3Spontaneous Fanconi syndrome in the dogMetabolism, Vol. 27, No. 1Renal response to phosphorus deprivation: Effect of the parathyroids and bicarbonateKidney International, Vol. 11, No. 5 More from this issue > Volume 227Issue 6December 1974Pages 1422-1427 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.6.1422PubMed4374094History Published online 1 December 1974 Published in print 1 December 1974 Metrics

Uptake, Storage, and Utilization of Phosphate by Yeast. I. Effects of Phosphate Depletion during Growth

(1966). Uptake, Storage, and Utilization of Phosphate by Yeast. I. Effects of Phosphate Depletion during Growth. Proceedings. Annual meeting - American Society of Brewing Chemists: Vol. 24, Proceedings of the Annual Meeting 1966, pp. 76-85.