Log in

Relevant bibliographies by topics / Phosphate depletion / Journal articles

To see the other types of publications on this topic, follow the link: Phosphate depletion.

Journal articles on the topic 'Phosphate depletion'

Author: Grafiati

Published: 31 May 2025

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Phosphate depletion.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

NAKAGAWA, TAKESHI, and PETER J. BUTTERWORTH. "Metabolic changes accompanying phosphate depletion." Biochemical Society Transactions 16, no. 5 (1988): 785. http://dx.doi.org/10.1042/bst0160785.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Pivnick, Enikö K., Natalie C. Kerr, Robert A. Kaufman, Deborah P. Jones, and Russell W. Chesney. "Rickets Secondary to Phosphate Depletion." Clinical Pediatrics 34, no. 2 (1995): 73–78. http://dx.doi.org/10.1177/000992289503400202.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Lakin-Thomas, P. L. "Evidence against a direct role for inositol phosphate metabolism in the circadian oscillator and the blue-light signal transduction pathway in Neurospora crassa." Biochemical Journal 292, no. 3 (1993): 813–18. http://dx.doi.org/10.1042/bj2920813.

Full text

Abstract:

The inositol-depletion hypothesis proposes that the effects of Li+ on cellular functions are the result of inhibition by Li+ of the inositol monophosphate phosphatase and subsequent depletion of inositol lipids. This mechanism has been proposed to account for the effects of Li+ on the period of the circadian oscillator. Inositol phosphate metabolism has also been proposed as part of the blue-light signal-transduction pathway through which the phase of the circadian oscillator can be reset by light pulses. Four predictions of these two hypotheses have been tested in the fungus Neurospora crassa

APA, Harvard, Vancouver, ISO, and other styles

4

Oh, H. Y., G. Z. Fadda, M. Smogorzewski, H. H. Liou, and S. G. Massry. "Phosphate depletion impairs leucine-induced insulin secretion." Journal of the American Society of Nephrology 5, no. 5 (1994): 1259–65. http://dx.doi.org/10.1681/asn.v551259.

Full text

Abstract:

Phosphate depletion (PD) in vivo causes a sundry of abnormalities in pancreatic islets including a rise in cytosolic calcium, low ATP content, reduced Ca2+ ATPase and Na(+)-K+ ATPase activity, and impaired insulin secretion in response to glucose or potassium. L-Leucine is a strong secretagogue that triggers insulin secretion by deamination to alpha-ketoisocaproic acid (KIC) and the subsequent metabolism of the latter to ATP and by the activation of glutamate dehydrogenase (GLDH), which acts on glutamate to generate alpha-ketoglutarate, the metabolism of which results in ATP production. The ge

APA, Harvard, Vancouver, ISO, and other styles

5

Fadda, G. Z., P. Thanakitcharu, and S. G. Massry. "Phosphate Depletion Reduces Potassium-Induced Insulin Secretion." Experimental Biology and Medicine 198, no. 2 (1991): 742–46. http://dx.doi.org/10.3181/00379727-198-43313.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Rifat, Dalin, William R. Bishai, and Petros C. Karakousis. "Phosphate Depletion: A Novel Trigger forMycobacterium tuberculosisPersistence." Journal of Infectious Diseases 200, no. 7 (2009): 1126–35. http://dx.doi.org/10.1086/605700.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Tanaka, T., T. F. Thingstad, T. Løvdal, et al. "Availability of phosphate for phytoplankton and bacteria and of labile organic carbon for bacteria at different pCO<sub>2</sub> levels in a mesocosm study." Biogeosciences Discussions 4, no. 6 (2007): 3937–60. http://dx.doi.org/10.5194/bgd-4-3937-2007.

Full text

Abstract:

Abstract. Availability of phosphate for phytoplankton and bacteria and of labile organic carbon for bacteria at different pCO2 levels were studied in a mesocosm experiment (PeECE III). Using nutrient-depleted SW Norwegian fjord waters, three different levels of pCO2 (350 μatm: 1×CO2; 750 μatm: 2×CO2; 1050 μatm: 3×CO2) were set up, and nitrate and phosphate were added at the start of the experiment in order to induce a phytoplankton bloom. Despite similar responses of total particulate P concentration and phosphate turnover time at the three different pCO2 levels, the size distribution of parti

APA, Harvard, Vancouver, ISO, and other styles

8

Chazot, Guillaume, Sandrine Lemoine, Gabriel Kocevar, et al. "Intracellular Phosphate and ATP Depletion Measured by Magnetic Resonance Spectroscopy in Patients Receiving Maintenance Hemodialysis." Journal of the American Society of Nephrology 32, no. 1 (2020): 229–37. http://dx.doi.org/10.1681/asn.2020050716.

Full text

Abstract:

BackgroundThe precise origin of phosphate that is removed during hemodialysis remains unclear; only a minority comes from the extracellular space. One possibility is that the remaining phosphate originates from the intracellular compartment, but there have been no available data from direct assessment of intracellular phosphate in patients undergoing hemodialysis.MethodsWe used phosphorus magnetic resonance spectroscopy to quantify intracellular inorganic phosphate (Pi), phosphocreatine (PCr), and βATP. In our pilot, single-center, prospective study, 11 patients with ESKD underwent phosphorus

APA, Harvard, Vancouver, ISO, and other styles

9

BONINI, Beatriz M., Christophe VAN VAECK, Christer LARSSON, et al. "Expression of Escherichia coli otsA in a Saccharomyces cerevisiae tps1 mutant restores trehalose 6-phosphate levels and partly restores growth and fermentation with glucose and control of glucose influx into glycolysis." Biochemical Journal 350, no. 1 (2000): 261–68. http://dx.doi.org/10.1042/bj3500261.

Full text

Abstract:

The TPS1 gene, encoding trehalose-6-phosphate synthase (TPS), exerts an essential control on the influx of glucose into glycolysis in the yeast Saccharomyces cerevisiae. The deletion of TPS1 causes an inability to grow on glucose because of a hyperaccumulation of sugar phosphates and depletion of ATP and phosphate. We show that expression of the Escherichia coli homologue, otsA, in a yeast tps1 mutant results in high TPS activity. Although the trehalose 6-phosphate (Tre6P) level during exponential growth on glucose was at least as high as in a wild-type yeast strain, growth on glucose was only

APA, Harvard, Vancouver, ISO, and other styles

10

Shuvy, Mony, Suzan Abedat, Ran Eliaz, et al. "Hyperphosphatemia is required for initiation but not propagation of kidney failure-induced calcific aortic valve disease." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 4 (2019): H695—H704. http://dx.doi.org/10.1152/ajpheart.00765.2018.

Full text

Abstract:

High serum levels of phosphate are associated with uremia-induced calcific aortic valve disease (CAVD). However, it is not clear whether hyperphosphatemia is required in all phases of the process. Our aim was to determine the effects of phosphate and phosphate depletion at different phases of valve disease. The experimental design consisted of administering a uremia-inducing diet, with or without phosphate enrichment, to rats for 7 wk. Forty-two rats were fed with a phosphate-enriched uremic regimen that caused renal insufficiency and hyperphosphatemia. Another 42 rats were fed with a phosphat

APA, Harvard, Vancouver, ISO, and other styles

11

Harmelin, D. L., F. I. R. Martin, and J. D. Wark. "Antacid-induced phosphate depletion syndrome presenting as nephrolithiasis." Australian and New Zealand Journal of Medicine 20, no. 6 (1990): 803–5. http://dx.doi.org/10.1111/j.1445-5994.1990.tb00427.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Massry, S. G., S. M. Hajjar, P. Koureta, G. Z. Fadda, and M. Smogorzewski. "Phosphate depletion increases cytosolic calcium of brain synaptosomes." American Journal of Physiology-Renal Physiology 260, no. 1 (1991): F12—F18. http://dx.doi.org/10.1152/ajprenal.1991.260.1.f12.

Full text

Abstract:

Phosphate depletion (PD) is associated with a rise in resting levels of [Ca2+]i in pancreatic islets. It is not known whether this derangement occurs in other cells, and the mechanisms by which PD affects [Ca2+]i have not been delineated. This study examined the effect of PD on [Ca2+]i of brain synaptosomes and evaluated potential mechanisms that may lead to rise in their [Ca2+]i. [Ca2+]i levels in synaptosomes of PD rats (460 +/- 18.3 nM) were higher (P less than 0.01) than those of pair-weighed (PW) rats (358 +/- 12.5 nM). Verapamil treatment of PD rats (PD-V) normalized [Ca2+]i in their syn

APA, Harvard, Vancouver, ISO, and other styles

13

Zhou, Xin-Jin, George Z. Fadda, Alessandra F. Perna, and Shaul G. Massry. "Phosphate depletion impairs insulin secretion by pancreatic islets." Kidney International 39, no. 1 (1991): 120–28. http://dx.doi.org/10.1038/ki.1991.15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Hum, Alan N., Graham C. Burdge, Sarah M. Wright, and Anthony D. Postle. "S phase depletion of nuclear CTP:choline phosphate cytidylyltransferase." Biochemical Society Transactions 26, no. 3 (1998): S222. http://dx.doi.org/10.1042/bst026s222.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Koppelaar, R. H. E. M., and H. P. Weikard. "Assessing phosphate rock depletion and phosphorus recycling options." Global Environmental Change 23, no. 6 (2013): 1454–66. http://dx.doi.org/10.1016/j.gloenvcha.2013.09.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Wu, J. "Phosphate Depletion in the Western North Atlantic Ocean." Science 289, no. 5480 (2000): 759–62. http://dx.doi.org/10.1126/science.289.5480.759.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Saxena, S., L. Dansby, and M. Allon. "Adaptation to Phosphate Depletion in Opossum Kidney Cells." Biochemical and Biophysical Research Communications 216, no. 1 (1995): 141–47. http://dx.doi.org/10.1006/bbrc.1995.2602.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Kobayashi, Takashi, Malcolm K. Robinson, Vickye Robinson, Eve Derosa, Douglas W. Wilmore, and Danny O. Jacobs. "Glutathione Depletion Alters Hepatocellular High-Energy Phosphate Metabolism." Journal of Surgical Research 54, no. 3 (1993): 189–95. http://dx.doi.org/10.1006/jsre.1993.1030.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Stamelou, Maria, Ulrich Pilatus, Alexander Reuss, et al. "In vivo Evidence for Cerebral Depletion in High-Energy Phosphates in Progressive Supranuclear Palsy." Journal of Cerebral Blood Flow & Metabolism 29, no. 4 (2009): 861–70. http://dx.doi.org/10.1038/jcbfm.2009.2.

Full text

Abstract:

Indirect evidence from laboratory studies suggests that mitochondrial energy metabolism is impaired in progressive supranuclear palsy (PSP), but brain energy metabolism has not yet been studied directly in vivo in a comprehensive manner in patients. We have used combined phosphorus and proton magnetic resonance spectroscopy to measure adenosine-triphosphate (ATP), adenosine-diphosphate (ADP), phosphorylated creatine, unphosphorylated creatine, inorganic phosphate and lactate in the basal ganglia and the frontal and occipital lobes of clinically probable patients ( N= 21; PSP stages II to III)

APA, Harvard, Vancouver, ISO, and other styles

20

Bushinsky, David A., Susan B. Smith, Konstantin L. Gavrilov, Leonid F. Gavrilov, Jianwei Li, and Riccardo Levi-Setti. "Chronic acidosis-induced alteration in bone bicarbonate and phosphate." American Journal of Physiology-Renal Physiology 285, no. 3 (2003): F532—F539. http://dx.doi.org/10.1152/ajprenal.00128.2003.

Full text

Abstract:

Chronic metabolic acidosis increases urinary calcium excretion without altering intestinal calcium absorption, suggesting that bone mineral is the source of the additional urinary calcium. In vivo and in vitro studies have shown that metabolic acidosis causes a loss of mineral calcium while buffering the additional hydrogen ions. Previously, we studied changes in femoral, midcortical ion concentrations after 7 days of in vivo metabolic acidosis induced by oral ammonium chloride. We found that, compared with mice drinking only distilled water, ammonium chloride induced a loss of bone sodium and

APA, Harvard, Vancouver, ISO, and other styles

21

Tanaka, T., T. F. Thingstad, T. Løvdal, et al. "Availability of phosphate for phytoplankton and bacteria and of glucose for bacteria at different <i>p</i>CO<sub>2</sub> levels in a mesocosm study." Biogeosciences 5, no. 3 (2008): 669–78. http://dx.doi.org/10.5194/bg-5-669-2008.

Full text

Abstract:

Abstract. Availability of phosphate for phytoplankton and bacteria and of glucose for bacteria at different pCO2 levels were studied in a mesocosm experiment (PeECE III). Using nutrient-depleted SW Norwegian fjord waters, three different levels of pCO2 (350 μatm: 1×CO2; 700 μatm: 2×CO2; 1050 μatm: 3×CO2) were set up, and nitrate and phosphate were added at the start of the experiment in order to induce a phytoplankton bloom. Despite similar responses of total particulate P concentration and phosphate turnover time at the three different pCO2 levels, the size distribution of particulate P and 3

APA, Harvard, Vancouver, ISO, and other styles

22

McPherson, C. D., G. N. Pierce, and W. C. Cole. "Ischemic cardioprotection by ATP-sensitive K+ channels involves high-energy phosphate preservation." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (1993): H1809—H1818. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1809.

Full text

Abstract:

We previously demonstrated that ATP-sensitive K+ channels (KATP) protect the guinea pig myocardium against ischemia-reperfusion injury (Cole et al., Circ. Res. 69: 571-581, 1991), but the cellular alterations leading to ischemic injury affected by KATP remain to be defined. This study investigates the relationship between activation of KATP and preservation of high-energy phosphates during global no-flow ischemia in arterially perfused guinea pig right ventricular walls. Electrical and mechanical activity were recorded via intracellular microelectrodes and a force transducer. Glibenclamide (10

APA, Harvard, Vancouver, ISO, and other styles

23

Lee, TCH, PL Chan, SJL Xu, and FWF Lee. "Comparison of growth and toxicity responses between non-toxic and toxic strains of Prorocentrum hoffmannianum." Aquatic Biology 29 (March 12, 2020): 59–70. http://dx.doi.org/10.3354/ab00725.

Full text

Abstract:

We aimed to study the growth and toxicity responses of non-toxic (CCMP683) and toxic (CCMP2804) strains of Prorocentrum hoffmannianum under various nitrate and phosphate concentrations. The 2 strains were cultured in L1-Si medium with standard, depleted or 10-fold repleted nitrate or phosphate. CCMP683 cultured in standard L1-Si medium exhibited delayed growth. Nitrate or phosphate depletion decreased the cell density of both strains. Repletion of nitrate slightly increased the cell density of both strains. Repletion of phosphate also slightly increased the cell density of CCMP2804 but surpris

APA, Harvard, Vancouver, ISO, and other styles

24

Poillon, WN, BC Kim, RJ Labotka, CU Hicks, and JA Kark. "Antisickling effects of 2,3-diphosphoglycerate depletion." Blood 85, no. 11 (1995): 3289–96. http://dx.doi.org/10.1182/blood.v85.11.3289.bloodjournal85113289.

Full text

Abstract:

Elevation of 2,3-bisphosphoglycerate (2,3-DPG) in sickle erthrocytes (SS RBCs) and concomitant acidification of the cell interior promote polymerization by decreasing the solubility (csat) of deoxyhemoglobin S. The antisickling effect of 2,3-DPG depletion was evaluated after activation of the 2,3-DPG phosphatase activity of bisphosphoglycerate mutase by glycolate-2-phosphate, leading to rapid loss of intracellular 2,3-DPG. To ensure its maximal reduction in a physiologic medium, isosmotic CO2/bicarbonate-buffered saline, pH 7.0, was used. Substitution of K+ for Na+ as the major extracellular c

APA, Harvard, Vancouver, ISO, and other styles

25

Clark, Gregory T., James Dunlop, and H. Thai Phung. "Phosphate absorption by Arabidopsis thaliana: interactions between phosphorus status and inhibition by arsenate." Functional Plant Biology 27, no. 10 (2000): 959. http://dx.doi.org/10.1071/pp99108.

Full text

Abstract:

The effects of phosphorus status and arsenate on the absorption of phosphate by roots of intact sterile seedlings of Arabidopsis thaliana were studied by analysing the rate of depletion of phosphate from solutions initially containing 10 M KH2PO4. Depletion of phosphate from the experimental solutions was measured both chemically and by labelling with 32P. There was a substantial efflux of phosphate coincident with a rapid influx of phosphate, with efflux increasing with increasing phosphorus status. The highest rates of absorption were obtained for the plants initially grown with a high level

APA, Harvard, Vancouver, ISO, and other styles

26

Breves, G., R. Ross, and H. Höller. "Dietary phosphorus depletion in sheep: effects on plasma inorganic phosphorus, calcium, l,25-(OH)2-Vit.D3 and alkaline phosphatase and on gastrointestinal P and Ga balances." Journal of Agricultural Science 105, no. 3 (1985): 623–29. http://dx.doi.org/10.1017/s0021859600059530.

Full text

Abstract:

SUMMARYExperiments were carried out to study the effects of dietary P depletion on plasma concentrations of inorganic P (P1), calcium, 1,25-(OH)2-Vit.D3 and alkaline phosphatase, and to investigate the effects of P depletion, in comparison with P repletion, on intestinal flow and net disappearance of Ca and P in sheep. The animals were adapted to an experimental diet of pellets and chopped straw providing between 0·91 and 1·04 g P/day for depletion. They were repleted by single infusions of phosphate into the duodenum raising total P supply to about 4·1 g/day. During P depletion plasma P1, con

APA, Harvard, Vancouver, ISO, and other styles

27

Kirk, C. J., G. Guillon, M. N. Balestre, and S. Jard. "Stimulation, by vasopressin and other agonists, of inositol-lipid breakdown and inositol phosphate accumulation in WRK 1 cells." Biochemical Journal 240, no. 1 (1986): 197–204. http://dx.doi.org/10.1042/bj2400197.

Full text

Abstract:

WRK 1 cells were labelled to equilibrium with 2-myo-[3H]inositol and stimulated with vasopressin. Within 3 s of hormone stimulation there was a marked accumulation of 3H-labelled InsP2 and InsP3 (inositol bis- and tris-phosphate), but not of InsP (inositol monophosphate). There was an associated, and rapid, depletion of 3H-labelled PtdInsP and PtdInsP2 (phosphatidylinositol mono- and bis-phosphates), but not of PtdIns (phosphatidylinositol), in these cells. Some 4% of the radioactivity in the total inositol lipid pool of WRK 1 cells was recovered in InsP2 and InsP3 after 10 s stimulation with

APA, Harvard, Vancouver, ISO, and other styles

28

PEARSON, M. P., L. L. SPRIET, and E. D. STEVENS. "EFFECT OF SPRINT TRAINING ON SWIM PERFORMANCE AND WHITE MUSCLE METABOLISM DURING EXERCISE AND RECOVERY IN RAINBOW TROUT (SALMO GAIRDNERI)." Journal of Experimental Biology 149, no. 1 (1990): 45–60. http://dx.doi.org/10.1242/jeb.149.1.45.

Full text

Abstract:

Experimental fish were sprint trained by individual chasing for 30 s on alternate days for 9 weeks. Ten trained and 10 untrained animals were rapidly freezeclamped at rest and 0, 1, 3 and 6h after a 5-min chase. Swimming speed of 10 fish in each group was measured in a 2-min chase. Phosphocreatine (PCr), creatine, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), glycogen, glucose-1-phosphate (G-l-P), glucose-6-phosphate (G-6-P), fructose-6-phosphate (Fru-6-P), glucose, glycerol-3-phosphate (Glyc-3- P), pyruvate and lactate were measured on extracts from

APA, Harvard, Vancouver, ISO, and other styles

29

Kiersztejn, M., I. Chervu, M. Smogorzewski, G. Z. Fadda, J. M. Alexiewicz, and S. G. Massry. "On the mechanisms of impaired phagocytosis in phosphate depletion." Journal of the American Society of Nephrology 2, no. 10 (1992): 1484–89. http://dx.doi.org/10.1681/asn.v2101484.

Full text

Abstract:

Phosphate depletion (PD) impairs the phagocytic ability of polymorphonuclear leukocytes (PMNL). This derangement has been attributed to the low ATP content of PMNL in PD. The mechanisms responsible for the low ATP content are not well defined. Phosphorus deficiency, per se, and/or other cellular metabolic consequences of PD such as a rise in cytosolic calcium ([Ca2+]i) could be responsible. Indeed, PD is associated with a rise in [Ca2+]i in other cells, and such an event may inhibit mitochondrial ATP production. It is also not evident whether the impaired phagocytosis in PD is due to low ATP c

APA, Harvard, Vancouver, ISO, and other styles

30

Smogorzewski, M., A. Islam, P. Koureta, G. Z. Fadda, and S. G. Massry. "Reduced phospholipid contents of brain synaptosomes in phosphate depletion." American Journal of Physiology-Endocrinology and Metabolism 261, no. 6 (1991): E742—E747. http://dx.doi.org/10.1152/ajpendo.1991.261.6.e742.

Full text

Abstract:

The effects of 6 wk phosphate depletion (PD) and pair-weight feeding (PW) without and with treatment with verapamil (PD-V and PW-V, respectively) on phospholipid (PL) and cholesterol content and on resting levels of cytosolic calcium concentration ([Ca2+]i) of brain synaptosomes of rats were examined. PD was associated with significantly (P less than 0.01) lower synaptosomal content of total PL, phosphatidylinositol (PI), phosphatidylserine (PS), and phosphatidylethanolamine (PE) and with significant (P less than 0.01) elevation in [Ca2+]i. Verapamil treatment of PD rats prevented the rise in

APA, Harvard, Vancouver, ISO, and other styles

31

Zhu, Yong-Guan, Timothy R. Cavagnaro, Sally E. Smith, and Sandy Dickson. "Backseat driving? Accessing phosphate beyond the rhizosphere-depletion zone." Trends in Plant Science 6, no. 5 (2001): 194–95. http://dx.doi.org/10.1016/s1360-1385(01)01957-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Håglin, Lena. "Using phosphate supplementation to reverse hypophosphatemia and phosphate depletion in neurological disease and disturbance." Nutritional Neuroscience 19, no. 5 (2015): 213–23. http://dx.doi.org/10.1179/1476830515y.0000000024.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Ohira, Y., K. Saito, T. Wakatsuki, et al. "Responses of beta-adrenoceptor in rat soleus to phosphorus compound levels and/or unloading." American Journal of Physiology-Cell Physiology 266, no. 5 (1994): C1257—C1262. http://dx.doi.org/10.1152/ajpcell.1994.266.5.c1257.

Full text

Abstract:

Responses of beta-adrenoceptor (beta-AR) in rat soleus to gravitational unloading and/or changes in the levels of phosphorus compounds by feeding either creatine or its analogue beta-guanidinopropionic acid (beta-GPA) were studied. A decrease in the density of beta-AR (about -35%) was induced by 10 days of hindlimb suspension, but the affinity of the receptor was unaffected. Suspension unloading tended to increase the levels of adenosine triphosphate and phosphocreatine and decrease inorganic phosphate. Even without unloading, the beta-AR density decreased after an oral creatine supplementatio

APA, Harvard, Vancouver, ISO, and other styles

34

Agius, Loranne. "Dietary carbohydrate and control of hepatic gene expression: mechanistic links from ATP and phosphate ester homeostasis to the carbohydrate-response element-binding protein." Proceedings of the Nutrition Society 75, no. 1 (2015): 10–18. http://dx.doi.org/10.1017/s0029665115002451.

Full text

Abstract:

Type 2 diabetes and non-alcoholic fatty liver disease (NAFLD) are associated with elevated hepatic glucose production and fatty acid synthesis (de novolipogenesis (DNL)). High carbohydrate diets also increase hepatic glucose production and lipogenesis. The carbohydrate-response element-binding protein (ChREBP, encoded byMLXIPL) is a transcription factor with a major role in the hepatic response to excess dietary carbohydrate. Because its target genes include pyruvate kinase (PKLR) and enzymes of lipogenesis, it is regarded as a key regulator for conversion of dietary carbohydrate to lipid for

APA, Harvard, Vancouver, ISO, and other styles

35

Venditti, Rossella, Maria Chiara Masone, Laura Rita Rega, et al. "The activity of Sac1 across ER–TGN contact sites requires the four-phosphate-adaptor-protein-1." Journal of Cell Biology 218, no. 3 (2019): 783–97. http://dx.doi.org/10.1083/jcb.201812021.

Full text

Abstract:

Phosphatidylinositol-4-phosphate (PI4P), a phosphoinositide with key roles in the Golgi complex, is made by Golgi-associated phosphatidylinositol-4 kinases and consumed by the 4-phosphatase Sac1 that, instead, is an ER membrane protein. Here, we show that the contact sites between the ER and the TGN (ERTGoCS) provide a spatial setting suitable for Sac1 to dephosphorylate PI4P at the TGN. The ERTGoCS, though necessary, are not sufficient for the phosphatase activity of Sac1 on TGN PI4P, since this needs the phosphatidyl-four-phosphate-adaptor-protein-1 (FAPP1). FAPP1 localizes at ERTGoCS, inter

APA, Harvard, Vancouver, ISO, and other styles

36

Maswoswe, S. M., F. Daneshmand, and D. R. Davies. "Metabolic effects of d-glyceraldehyde in isolated hepatocytes." Biochemical Journal 240, no. 3 (1986): 771–76. http://dx.doi.org/10.1042/bj2400771.

Full text

Abstract:

The effects of D-glyceraldehyde on the hepatocyte contents of various metabolites were examined and compared with the effects of fructose, glycerol and dihydroxyacetone, which all enter the glycolytic/gluconeogenic pathways at the triose phosphate level. D-Glyceraldehyde (10 MM) caused a substantial depletion of hepatocyte ATP, as did equimolar concentrations of fructose and glycerol. D-Glyceraldehyde and fructose each caused a 2-fold increase in fructose 1,6-bisphosphate and the accumulation of millimolar quantities of fructose 1-phosphate in the cells. D-Glyceraldehyde caused an increase in

APA, Harvard, Vancouver, ISO, and other styles

37

Kobryn, C. E., and L. J. Mandel. "Decreased protein phosphorylation induced by anoxia in proximal renal tubules." American Journal of Physiology-Cell Physiology 267, no. 4 (1994): C1073—C1079. http://dx.doi.org/10.1152/ajpcell.1994.267.4.c1073.

Full text

Abstract:

Anoxia-induced depletion of cellular ATP may affect the degree of protein phosphorylation due to kinase inhibition. In this study, protein phosphorylation was measured in rabbit kidney proximal tubules under normoxic or anoxic conditions in a medium containing 32P. During the first 20 min of normoxia, phosphate incorporation was linear, averaging 17 +/- 5 pmol.mg protein-1.min-1 and was 70% inhibited by the protein kinase C inhibitor chelerythrine chloride. Phosphorylation measurements initiated simultaneously with anoxic conditions (95% N2-5% CO2) significantly reduced the initial rate to 58%

APA, Harvard, Vancouver, ISO, and other styles

38

Blair-West, J. R., D. A. Denton, M. J. McKinley, B. G. Radden, E. H. Ramshaw, and J. D. Wark. "Behavioral and tissue responses to severe phosphorus depletion in cattle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (1992): R656—R663. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r656.

Full text

Abstract:

Two-year-old Aberdeen Angus heifers were depleted of phosphorus (P) by loss of phosphate in saliva from a parotid gland fistula combined with a low-P diet. The inorganic phosphate concentrations (Pi) of plasma, parotid saliva, ruminal fluid, and feces were reduced, but cerebrospinal fluid Pi was unaltered. Plasma Pi fell to less than 1.0 mM in 12 wk, and the cows displayed an avid appetite for old bones. P-deficient cows preferred old weathered bones to fresh bones until the latter had aged for approximately 1.5 yr. They did not eat blood, peritoneal fat, or meat, fresh or aged for 2-3 yr. The

APA, Harvard, Vancouver, ISO, and other styles

39

Schaffer, Stephen W., and Boen H. Tan. "Effect of calcium depletion and calcium paradox on myocardial energy metabolism." Canadian Journal of Physiology and Pharmacology 63, no. 11 (1985): 1384–91. http://dx.doi.org/10.1139/y85-228.

Full text

Abstract:

Both phases of the calcium paradox were associated with major alterations in myocardial energy metabolism. During calcium-free perfusion contractility of the heart ceased, resulting in a dramatic decrease in anaerobic and aerobic metabolism but no change in tissue high energy phosphate levels. Tissue content of most citric acid cycle intermediates were elevated, while there was a net decrease in the content of transaminase-linked amino acids. Reperfusion of the calcium-depleted heart with calcium-containing buffer failed to restore either the contractile or the metabolic state of the heart. Wi

APA, Harvard, Vancouver, ISO, and other styles

40

M'Zali, H., and F. Giraud. "Phosphoinositide reorganization in human erythrocyte membrane upon cholesterol depletion." Biochemical Journal 234, no. 1 (1986): 13–20. http://dx.doi.org/10.1042/bj2340013.

Full text

Abstract:

The effect of cholesterol depletion on the activity of phosphatidylinositol/phosphatidylinositol 4-phosphate and diacylglycerol kinases and polyphosphoinositide phosphodiesterase has been studied in isolated membranes of human normal and cholesterol-depleted erythrocytes. Polyphosphoinositide synthesis (phosphatidylinositol/phosphatidylinositol 4-phosphate kinase activities) were found to depend on the permeability and sidedness characteristics of the membrane vesicles, which could limit the accessibility of ATP for the enzymes. When measured under proper conditions, phosphatidylinositol 4-pho

APA, Harvard, Vancouver, ISO, and other styles

41

Grünberg, W., J. A. Mol, and E. Teske. "Red Blood Cell Phosphate Concentration and Osmotic Resistance During Dietary Phosphate Depletion in Dairy Cows." Journal of Veterinary Internal Medicine 29, no. 1 (2014): 395–99. http://dx.doi.org/10.1111/jvim.12497.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Green, J., O. Foellmer, C. R. Kleeman, and M. M. Basic. "Acute phosphate depletion inhibits the Na+/H+ antiporter in a cultured renal cell line." American Journal of Physiology-Renal Physiology 265, no. 3 (1993): F440—F448. http://dx.doi.org/10.1152/ajprenal.1993.265.3.f440.

Full text

Abstract:

We studied the effect of acute Pi depletion on the regulation of intracellular pH (pHi) in the OK opossum kidney cell line by using the pH-sensitive dye 2'7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Cell recovery from an NH4Cl acid load in HCO3-free buffer disclosed an Na(+)-dependent component blocked by amiloride and a smaller Na(+)-independent component that increased on exposure of the cells to a high-K+ buffer. After 24-h incubation of the cells in phosphate-free medium, pHi recovery by the Na+/H+ exchanger was markedly inhibited, whereas the Na(+)-independent pHi recovery was n

APA, Harvard, Vancouver, ISO, and other styles

43

Bushinsky, David A., Susan B. Smith, Konstantin L. Gavrilov, Leonid F. Gavrilov, Jianwei Li, and Riccardo Levi-Setti. "Acute acidosis-induced alteration in bone bicarbonate and phosphate." American Journal of Physiology-Renal Physiology 283, no. 5 (2002): F1091—F1097. http://dx.doi.org/10.1152/ajprenal.00155.2002.

Full text

Abstract:

During an acute fall in systemic pH due to a decrease in the concentration of serum bicarbonate ([HCO[Formula: see text]]), metabolic acidosis, there is an influx of hydrogen ions into the mineral phase of bone, buffering the decrement in pH. When bone is cultured in medium modeling acute metabolic acidosis, the influx of hydrogen ions is coupled to an efflux of sodium and potassium and a depletion of mineral carbonate. These ionic fluxes would be expected to neutralize some of the excess hydrogen ions and restore the pH toward normal. Approximately one-third of bone carbonate is located on th

APA, Harvard, Vancouver, ISO, and other styles

44

Seifert, Erin, Gyorgy Hajnoczky, Cesar Vasquez-Trincado, et al. "Mitochondrial phosphate carrier depletion in skeletal muscle and Ca2+ homeostasis." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1865 (September 2024): 149160. http://dx.doi.org/10.1016/j.bbabio.2024.149160.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Hill, Andrew G., Wee Teo, Andrew Still, Bryan R. Parry, Lindsay D. Plank, and Graham L. Hill. "CELLULAR POTASSIUM DEPLETION PREDISPOSES TO HYPOKALAEMIA AFTER ORAL SODIUM PHOSPHATE." ANZ Journal of Surgery 68, no. 12 (1998): 856–58. http://dx.doi.org/10.1111/j.1445-2197.1998.tb04702.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Smogorzewski, Miroslaw, Anisul Islam, Pany Koureta, and Shaul G. Massry. "Abnormal Norepinephrine Metabolism in Rat Brain Synaptosomes in Phosphate Depletion." American Journal of Nephrology 13, no. 1 (1993): 43–52. http://dx.doi.org/10.1159/000168587.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Latta, Markus, Gerald Künstle, Marcel Leist, and Albrecht Wendel. "Metabolic Depletion of Atp by Fructose Inversely Controls Cd95- and Tumor Necrosis Factor Receptor 1–Mediated Hepatic Apoptosis." Journal of Experimental Medicine 191, no. 11 (1999): 1975–86. http://dx.doi.org/10.1084/jem.191.11.1975.

Full text

Abstract:

Hepatocyte apoptosis is crucial in several forms of liver disease. Here, we examined in different models of murine liver injury whether and how metabolically induced alterations of hepatocyte ATP levels control receptor-mediated apoptosis. ATP was depleted either in primary hepatocytes or in vivo by various phosphate-trapping carbohydrates such as fructose. After the activation of the tumor necrosis factor (TNF) receptor or CD95, the extent of hepatocyte apoptosis and liver damage was quantified. TNF-induced cell death was completely blocked in ATP-depleted hepatocyte cultures, whereas apoptos

APA, Harvard, Vancouver, ISO, and other styles

48

Mousson de camaret, Bénédicte, Jan-Willem Taanman, Sylvie Padet, et al. "Kinetic properties of mutant deoxyguanosine kinase in a case of reversible hepatic mtDNA depletion." Biochemical Journal 402, no. 2 (2007): 377–85. http://dx.doi.org/10.1042/bj20060705.

Full text

Abstract:

DGUOK [dG (deoxyguanosine) kinase] is one of the two mitochondrial deoxynucleoside salvage pathway enzymes involved in precursor synthesis for mtDNA (mitochondrial DNA) replication. DGUOK is responsible for the initial rate-limiting phosphorylation of the purine deoxynucleosides, using a nucleoside triphosphate as phosphate donor. Mutations in the DGUOK gene are associated with the hepato-specific and hepatocerebral forms of MDS (mtDNA depletion syndrome). We identified two missense mutations (N46S and L266R) in the DGUOK gene of a previously reported child, now 10 years old, who presented wit

APA, Harvard, Vancouver, ISO, and other styles

49

Armstrong, RD, and KR Helyar. "Changes in soil phosphate fractions in the rhizosphere of semi-arid pasture grasses." Soil Research 30, no. 2 (1992): 131. http://dx.doi.org/10.1071/sr9920131.

Full text

Abstract:

The comparative ability of several species of grass common to the semi-arid mulga shrublands of south-western Queensland, namely Cenchrus ciliaris cv. U.S.A., Aristida armata, Digitaria ammophilla and Thyridolepis mitchelliana, to deplete various fractions of soil inorganic/organic phosphorus was assessed using a rhizosphere thin section methodology. All species significantly depleted inorganic phosphorus extractable with 0.5 M NaHCO3, 0.1 M NaOH, and 1.0 M HCl. The grasses were able to deplete 39, 32, and 29%, respectively, of the inorganic component of each of these extracts. In contrast, th

APA, Harvard, Vancouver, ISO, and other styles

50

Lee, Thomas Chun-Hung, Kaze King-Yip Lai, Steven Jing-Liang Xu, and Fred Wang-Fat Lee. "Upregulation of Peridinin-Chlorophyll A-Binding Protein in a Toxic Strain of Prorocentrum hoffmannianum under Normal and Phosphate-Depleted Conditions." International Journal of Molecular Sciences 24, no. 2 (2023): 1735. http://dx.doi.org/10.3390/ijms24021735.

Full text

Abstract:

Some strains of the dinoflagellate species Prorocentrum hoffmannianum show contrasting ability to produce diarrhetic shellfish poisoning (DSP) toxins. We previously compared the okadaic acid (OA) production level between a highly toxic strain (CCMP2804) and a non-toxic strain (CCMP683) of P. hoffmannianum and revealed that the cellular concentration of OA in CCMP2804 would increase significantly under the depletion of phosphate. To understand the molecular mechanisms, here, we compared and analyzed the proteome changes of both strains growing under normal condition and at phosphate depletion u

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!