Mobility of inorganic and organic phosphorus forms under different levels of phosphate and poultry litter fertilization in soils

The eutrophication of aquifers is strongly linked to the mobility of P in soils. Although P mobility was considered irrelevant in a more distant past, more recent studies have shown that P, both in organic (Po) and inorganic forms (Pi), can be lost by leaching and eluviation through the soil profile, particularly in less weathered and/or sandier soils with low P adsorption capacity. The purpose of this study was to determine losses of P forms by leaching and eluviation from soil columns. Each column consisted of five PVC rings (diameter 5 cm, height 10 cm), filled with two soil types: a clayey Red-Yellow Latosol and a sandy loam Red-Yellow Latosol, which were exposed to water percolation. The soils were previously treated with four P rates (as KH2PO4 ) to reach 0, 12.5, 25.0 and 50 % of the maximum P adsorption capacity (MPAC). The P source was homogenized with the whole soil volume and incubated for 60 days. After this period the soils were placed in the columns; the soil of the top ring was mixed with five poultry litter rates of 0, 20, 40, 80, and 160 t ha-1 (dry weight basis). Treatments consisted of a 4 x 5 x 2 factorial scheme corresponding to four MPAC levels, five poultry litter rates, two soils, with three replications, arranged in a completely randomized block design. Deionized water was percolated through the columns 10 times in 35 days to simulate about 1,200 mm rainfall. In the leachate of each column the inorganic P (reactive P, Pi) and organic P forms (unreactive P, Po) were determined. At the end of the experiment, the columns were disassembled and P was extracted with the extractants Mehlich-1 (HCl 0.05 mol L-1 and H2SO4 0.0125 mol L-1) and Olsen (NaHCO3 0.5 mol L-1; pH 8.5) from the soil of each ring. The Pi and Po fractions were measured by the Olsen extractant. It was found that under higher poultry litter rates the losses of unreactive P (Po) were 6.4 times higher than of reactive P (Pi). Both the previous P fertilization and increasing poultry litter rates caused a vertical movement of P down the soil columns, as verified by P concentrations extracted by Mehlich-1 and NaHCO3 (Olsen). The environmental critical level (ECL), i.e., the P soil concentration above which P leaching increases exponentially, was 100 and 150 mg dm-3 by Mehlich-1 and 40 and 60 mg dm-3 by Olsen, for the sandy loam and clay soils, respectively. In highly weathered soils, where residual P is accumulated by successive crops, P leaching through the profile can be significant, particularly when poultry litter is applied as fertilizer.

Fructose and glucose co-ingestion during prolonged exercise increases lactate and glucose fluxes and oxidation compared with an equimolar intake of glucose

BACKGROUND: When fructose is ingested together with glucose (GLUFRU) during exercise, plasma lactate and exogenous carbohydrate oxidation rates are higher than with glucose alone. OBJECTIVE: The objective was to investigate to what extent GLUFRU increased lactate kinetics and oxidation rate and gluconeogenesis from lactate (GNG(L)) and from fructose (GNG(F)). DESIGN: Seven endurance-trained men performed 120 min of exercise at approximately 60% VOmax (maximal oxygen consumption) while ingesting 1.2 g glucose/min + 0.8 g of either glucose or fructose/min (GLUFRU). In 2 trials, the effects of glucose and GLUFRU on lactate and glucose kinetics were investigated with glucose and lactate tracers. In a third trial, labeled fructose was added to GLUFRU to assess fructose disposal. RESULTS: In GLUFRU, lactate appearance (120 +/- 6 mumol . kg(1) . min(1)), lactate disappearance (121 +/- 7 mumol . kg(1) . min(1)), and oxidation (127 +/- 12 mumol . kg(1) . min(1)) rates increased significantly (P < 0.001) in comparison with glucose alone (94 +/- 16, 95 +/- 16, and 97 +/- 16 mumol . kg(1) . min(1), respectively). GNG(L) was negligible in both conditions. In GLUFRU, GNG(F) and exogenous fructose oxidation increased with time and leveled off at 18.8 +/- 3.7 and 38 +/- 4 mumol . kg(1) . min(1), respectively, at 100 min. Plasma glucose appearance rate was significantly higher (P < 0.01) in GLUFRU (91 +/- 6 mumol . kg(1) . min(1)) than in glucose alone (82 +/- 9 mumol . kg(1) . min(1)). Carbohydrate oxidation rate was higher (P < 0.05) in GLUFRU. CONCLUSIONS: Fructose increased total carbohydrate oxidation, lactate production and oxidation, and GNG(F). Fructose oxidation was explained equally by fructose-derived lactate and glucose oxidation, most likely in skeletal and cardiac muscle. This trial was registered at clinicaltrials.gov as NCT01128647.

Exudative mineral losses after serious burns: a clue to the alterations of magnesium and phosphate metabolism.

Hypomagnesemia and hypophosphatemia are frequent after severe burns; however, increased urinary excretion does not sufficiently explain the magnitude of the mineral depletion. We measured the mineral content of cutaneous exudates during the first week after injury. Sixteen patients aged 34 +/- 9 y (mean +/- SD) with thermal burns were studied prospectively and divided in 3 groups according to the extent of their burn injury and the presence or absence of mineral supplements: group 1 (n = 5), burns covering 26 +/- 5% of body surface; group 2 (n = 6), burns covering 41 +/- 10%; and group 3 (n = 5), burns covering 42 +/- 6% with prescription of magnesium and phosphate supplements. Cutaneous exudates were extracted from the textiles (surgical drapes, dressings, sheets, etc) surrounding the patients from day 1 to day 7 after injury. Mean magnesium serum concentrations decreased below reference ranges in 12 patients between days 1 and 4 and normalized thereafter. Phosphate, normal on day 0, was low during the first week. Albumin concentrations, normal on day 0, decreased and remained low. Urinary magnesium and phosphate excretion were within reference ranges and not larger in group 3. Mean daily cutaneous losses were 16 mmol Mg/d and 11 mmol P/d (largest in group 2). Exudative magnesium losses were correlated with burn severity (r = 0.709, P = 0.003). Cutaneous magnesium losses were nearly four times larger than urinary losses whereas cutaneous phosphate losses were smaller than urinary phosphate losses. Mean daily losses of both magnesium and phosphate were more than the recommended dietary allowances. Exudative losses combined with urinary losses largely explained the increased mineral requirements after burn injury.

Effect of bicarbonate and lactate buffer on glucose and lactate metabolism during hemodiafiltration in patients with multiple organ failure.

OBJECTIVE: To compare the effects of sodium bicarbonate and lactate for continuous veno-venous hemodiafiltration (CVVHDF) in critically ill patients. DESIGN AND SETTINGS: Prospective crossed-over controlled trial in the surgical and medical ICUs of a university hospital. PATIENTS: Eight patients with multiple organ dysfunction syndrome (MODS) requiring CVVHDF. INTERVENTION: Each patient received the two buffers in a randomized sequence over two consecutive days. MEASUREMENTS AND RESULTS: The following variables were determined: acid-base parameters, lactate production and utilization ((13)C lactate infusion), glucose turnover (6,6(2)H(2)-glucose), gas exchange (indirect calorimetry). No side effect was observed during lactate administration. Baseline arterial acid-base variables were equal with the two buffers. Arterial lactate (2.9 versus 1.5 mmol/l), glycemia (+18%) and glucose turnover (+23%) were higher in the lactate period. Bicarbonate and glucose losses in CVVHDF were substantial, but not lactate elimination. Infusing (13)C lactate increased plasma lactate levels equally with the two buffers. Lactate clearance (7.8+/-0.8 vs 7.5+/-0.8 ml/kg per min in the bicarbonate and lactate periods) and endogenous production rates (14.0+/-2.6 vs 13.6+/-2.6 mmol/kg per min) were similar. (13)C lactate was used as a metabolic substrate, as shown by (13)CO(2) excretion. Glycemia and metabolic rate increased significantly and similarly during the two periods during lactate infusion. CONCLUSION: Lactate was rapidly cleared from the blood of critically ill patients without acute liver failure requiring CVVHDF, being transformed into glucose or oxidized. Lactate did not exert undesirable effects, except moderate hyperglycemia, and achieved comparable effects on acid-base balance to bicarbonate.

Kinetics of dexamethasone-induced alterations of glucose metabolism in healthy humans.

Six healthy human subjects were studied during three 75-g oral, [13C]glucose tolerance tests to assess the kinetics of dexamethasone-induced impairment of glucose tolerance. On one occasion, they received dexamethasone (4 x 0.5 mg/day) during the previous 2 days. On another occasion, they received a single dose (0. 5 mg) of dexamethasone 150 min before ingestion of the glucose load. On the third occasion, they received a placebo. Postload plasma glucose was significantly increased after both 2 days dexamethasone and single dose dexamethasone compared with control (P < 0.05). This corresponded to a 20-23% decrease in the metabolic clearance rate of glucose, whereas total glucose turnover ([6,6-2H]glucose), total (indirect calorimetry) and exogenous glucose oxidation (13CO2 production), and suppression of endogenous glucose production were unaffected by dexamethasone. Plasma insulin concentrations were increased after 2 days of dexamethasone but not after a single dose of dexamethasone. In a second set of experiments, the effect of a single dose of dexamethasone on insulin sensitivity was assessed in six healthy humans during a 2-h euglycemic hyperinsulinemic clamp. Dexamethasone did not significantly alter insulin sensitivity. It is concluded that acute administration of dexamethasone impairs oral glucose tolerance without significantly decreasing insulin sensitivity.

Relation entre glucose cérébral et systémique chez le sujet neurolésé: une étude par microdialyse cérébrale

Introduction: Le glucose est le principal substrat énergétique cérébral. Sa concentration dans le cerveau est étroitement liée à la glycémie. Chez le patient neurolésé, du fait de l'augmentation des besoins énergétiques, les réserves cérébrales de glucose sont limitées. Une glycémie suffisamment élevée paraît nécessaire pour assurer un apport adéquat de glucose au cerveau. Objectifs : Le but de cette étude est de mieux comprendre la relation entre glucose cérébral et glycémie lors de lésion cérébrale en analysant la physiologie cérébrale chez des patients neurolésés. Plus précisément nous investiguerons: La relation entre le glucose cérébral et le glucose systémique et son association avec le pronostic vital, l'association entre la neuroglucopénie et différents paramètres cérébraux tel que l'hypertension intracrânienne (HTIC) ou la dysfonction énergétique et finalement l'effet d'une perfusion de glucose 10% sur le glucose cérébral lors d'état de neuroglucopénie. Méthodologie : Analyse d'une base de données prospective comportant des patients souffrant d'un traumatisme crânio-cérébral (TCC) ou une hémorragie sous- arachnoïdienne (HSA) sévères. Les patients comateux sont monitorés par un dispositif intra-parenchymateux avancé, comprenant un cathéter de microdialyse cérébrale et un capteur de PbO2. Résultats : 34 patients consécutifs (moyenne d'âge 42 ans, moyenne de temps jusqu'au début du monitoring : 1.5 jours ± 1 ; moyenne de la durée maximale du monitoring : 6 jours ± 3) ont été étudiés, 25 patients souffrant d'un TCC et 9 patients avec une HSA. Nous avons obtenu une corrélation individuelle entre le glucose cérébral et la glycémie chez 52.9 % des patients. Lorsque la glycémie est inférieure à 5 mmol/l, on observe plus fréquemment des épisodes de neuroglucopénie en comparaison aux valeurs intermédiaires de glycémie (5 - 9.9 mmol/l). Les épisodes d'HTIC (pression intracrânienne (PIC) > 20 mmHg) sont plus fréquemment associés à des épisodes de neuroglucopénie que lorsque la pression intracrânienne est normale 75 % vs. 35%. La dysfonction énergétique est plus souvent associés à des épisodes de neuroglucopénie que lorsque le LPR est normal: 55% contre 36%. Un coefficient de corrélation entre glucose cérébral et glycémie significativement plus élevé a été obtenu chez les survivants que chez les non-survivants (0.1 [interquartile range 0.02- 0.3] contre 0.32 [0.17-0.61]). Chez les patients neuroglucopéniques ayant une corrélation entre glucose cérébral et glycémie, la perfusion de glucose i.v. fait monter le glucose cérébral jusqu'à l'arrêt de la perfusion. Conclusion : Malgré une étroite relation entre glycémie et glucose cérébral en conditions stables, cette relation peut être altérée par des causes cérébrales chez les patients neurolésés montrant que la diminution de la disponibilité du glucose extracellulaire ne résulte pas uniquement d'une hypoglycémie relative mais également de causes cérébrales tel que l'hypoperfusion, l'HTIC ou la dysfonction énergétique.

Competitive sorption and desorption of phosphate and citrate in clayey and sandy loam soils

The increase of organic acids in soils can reduce phosphorus sorption. The objective of the study was to evaluate the competitive sorption of P and citrate in clayey and sandy loam soils, using a stirred-flow system. Three experiments were performed with soil samples (0-20 cm layer) of clayey (RYL-cl) and sandy loam (RYL-sl) Red Yellow Latosols (Oxisols). In the first study, the treatments were arranged in a 2 × 5 factorial design, with two soil types and five combinations of phosphorus and citrate application (only P; P + citrate; and citrate applied 7, 22, 52 min before P); in the second, the treatments were arranged in a 2 × 2 factorial design, corresponding to two soils and two forms of P and citrate application (only citrate and citrate + P); and in the third study, the treatments in a 2 × 2 × 6 factorial design consisted of two soils, two extractors (citrate and water) and six incubation times. In the RYL-cl and RYL-sl, P sorption was highest (44 and 25 % of P application, respectively), in the absence of citrate application. Under citrate application, P sorption was reduced in all treatments. The combined application of citrate and P reduced P sorption to 25.8 % of the initially applied P in RYL-cl and to 16.7 % in RYL-sl, in comparison to P without citrate. Citrate sorption in RYL-cl and RYL-sl was highest in the absence of P application, corresponding to 32.0 and 30.2 % of the citrate applied, respectively. With P application, citrate sorption was reduced to 26.4 and 19.7 % of the initially applied citrate in RYL-cl and RYL-sl, respectively. Phosphorus desorption was greater when citrate was used. Phosphorus desorption with citrate and water was higher in the beginning (until 24 h of incubation of P) in RYL-cl and RYL-sl, indicating a rapid initial phase, followed by a slow release phase. This suggests that according to the contact time of P with the soil colloids, the previously adsorbed P can be released to the soil solution in the presence of competing ligands such as citrate. In conclusion, a soil management with continuous input of organic acids is desirable, in view of their potential to compete for P sorption sites, especially in rather weathered soils.

Portal glucose infusion in the mouse induces hypoglycemia: evidence that the hepatoportal glucose sensor stimulates glucose utilization.

To analyze the role of the murine hepatoportal glucose sensor in the control of whole-body glucose metabolism, we infused glucose at a rate corresponding to the endogenous glucose production rate through the portal vein of conscious mice (Po-mice) that were fasted for 6 h. Mice infused with glucose at the same rate through the femoral vein (Fe-mice) and mice infused with a saline solution (Sal-mice) were used as controls. In Po-mice, hypoglycemia progressively developed until glucose levels dropped to a nadir of 2.3 +/- 0.1 mmol/l, whereas in Fe-mice, glycemia rapidly and transiently developed, and glucose levels increased to 7.7 +/- 0.6 mmol/l before progressively returning to fasting glycemic levels. Plasma insulin levels were similar in both Po- and Fe-mice during and at the end of the infusion periods (21.2 +/- 2.2 vs. 25.7 +/- 0.9 microU/ml, respectively, at 180 min of infusion). The whole-body glucose turnover rate was significantly higher in Po-mice than in Fe-mice (45.9 +/- 3.8 vs. 37.7 +/- 2.0 mg x kg(-1) x min)-1), respectively) and in Sal-mice (24.4 +/- 1.8 mg x kg(-1) x min(-1)). Somatostatin co-infusion with glucose in Po-mice prevented hypoglycemia without modifying the plasma insulin profile. Finally, tissue glucose clearance, which was determined after injecting 14C-2-deoxyglucose, increased to a higher level in Po-mice versus Fe-mice in the heart, brown adipose tissue, and the soleus muscle. Our data show that stimulation of the hepatoportal glucose sensor induced hypoglycemia and increased glucose utilization by a combination of insulin-dependent and insulin-independent or -sensitizing mechanisms. Furthermore, activation of the glucose sensor and/or transmission of its signal to target tissues can be blocked by somatostatin.

Effects of infused amino acids and lipids on glucose metabolism in healthy lean humans.

The effects of infusion of a triglyceride emulsion (which induces peripheral insulin resistance) and amino acids (which stimulate gluconeogenesis) on glucose metabolism were investigated in healthy lean humans during exogenous infusion of glucose. One group of subjects (n = 5) was infused for 7.5 h with 11.1 mumol/kg/min glucose; during the last 4 h, amino acids were also infused at a rate of 3.33 mg/kg/min. A second group of subjects (n = 5) was infused with glucose+lipids (Lipovenös, 10% 10 ml/min) for 7.5 h and amino acids were added during the last 4 h. Infusion of lipids suppressed the increase in glucose oxidation observed during infusion of glucose alone (delta glucose oxidation: -2.1 +/- 1.1 vs. + 4.5 +/- 1.4 mumol/kg/min; P < 0.05) and during infusion of glucose+amino acids (delta glucose oxidation: + 1.6 +/- 1.4 vs. + 10.6 +/- 1.2 mumol/kg/min; P < 0.05). Gluconeogenesis (determined from 13C glucose synthesis during infusion of 13C bicarbonate) increased from 1.1 +/- 0.2 mumol/kg/min during infusion of glucose and 1.6 +/- 0.3 during infusion of glucose+lipids to 3.2 +/- 0.4 and 3.1 +/- 0.4, respectively, when amino acid infusion was superimposed (P < 0.05 in both instances). Plasma glucose concentrations were identical during infusion of glucose alone or glucose+amino acids, with or without lipids. Insulin concentrations were significantly increased by lipids both during infusion of glucose alone and of glucose+amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans.

OBJECTIVE: To assess how intrahepatic fat and insulin resistance relate to daily fructose and energy intake during short-term overfeeding in healthy subjects. DESIGN AND METHODS: The analysis of the data collected in several studies in which fasting hepatic glucose production (HGP), hepatic insulin sensitivity index (HISI), and intrahepatocellular lipids (IHCL) had been measured after both 6-7 days on a weight-maintenance diet (control, C; n = 55) and 6-7 days of overfeeding with 1.5 (F1.5, n = 7), 3 (F3, n = 17), or 4 g fructose/kg/day (F4, n = 10), with 3 g glucose/kg/day (G3, n = 11), or with 30% excess energy as saturated fat (fat30%, n = 10). RESULTS: F3, F4, G3, and fat30% all significantly increased IHCL, respectively by 113 ± 86, 102 ± 115, 59 ± 92, and 90 ± 74% as compared to C (all P < 0.05). F4 and G3 increased HGP by 16 ± 10 and 8 ± 11% (both P < 0.05), and F3 and F4 significantly decreased HISI by 20 ± 22 and 19 ± 14% (both P < 0.01). In contrast, there was no significant effect of fat30% on HGP or HISI. CONCLUSIONS: Short-term overfeeding with fructose or glucose decreases hepatic insulin sensitivity and increases hepatic fat content. This indicates short-term regulation of hepatic glucose metabolism by simple carbohydrates.

Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: a microdialysis study.

OBJECTIVES: To analyze the effect of tight glycemic control with the use of intensive insulin therapy on cerebral glucose metabolism in patients with severe brain injury. DESIGN: Retrospective analysis of a prospective observational cohort. SETTING: University hospital neurologic intensive care unit. PATIENTS: Twenty patients (median age 59 yrs) monitored with cerebral microdialysis as part of their clinical care. INTERVENTIONS: Intensive insulin therapy (systemic glucose target: 4.4-6.7 mmol/L [80-120 mg/dL]). MEASUREMENTS AND MAIN RESULTS: Brain tissue markers of glucose metabolism (cerebral microdialysis glucose and lactate/pyruvate ratio) and systemic glucose were collected hourly. Systemic glucose levels were categorized as within the target "tight" (4.4-6.7 mmol/L [80-120 mg/dL]) vs. "intermediate" (6.8-10.0 mmol/L [121-180 mg/dL]) range. Brain energy crisis was defined as a cerebral microdialysis glucose <0.7 mmol/L with a lactate/pyruvate ratio >40. We analyzed 2131 cerebral microdialysis samples: tight systemic glucose levels were associated with a greater prevalence of low cerebral microdialysis glucose (65% vs. 36%, p < 0.01) and brain energy crisis (25% vs.17%, p < 0.01) than intermediate levels. Using multivariable analysis, and adjusting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentration (adjusted odds ratio 1.23, 95% confidence interval [CI] 1.10-1.37, for each 1 mmol/L decrease, p < 0.001) and insulin dose (adjusted odds ratio 1.10, 95% CI 1.04-1.17, for each 1 U/hr increase, p = 0.02) independently predicted brain energy crisis. Cerebral microdialysis glucose was lower in nonsurvivors than in survivors (0.46 +/- 0.23 vs. 1.04 +/- 0.56 mmol/L, p < 0.05). Brain energy crisis was associated with increased mortality at hospital discharge (adjusted odds ratio 7.36, 95% CI 1.37-39.51, p = 0.02). CONCLUSIONS: In patients with severe brain injury, tight systemic glucose control is associated with reduced cerebral extracellular glucose availability and increased prevalence of brain energy crisis, which in turn correlates with increased mortality. Intensive insulin therapy may impair cerebral glucose metabolism after severe brain injury.

Glucose uptake, utilization, and signaling in GLUT2-null islets.

We previously reported that pancreatic islet beta-cells from GLUT2-null mice lost the first phase but preserved the second phase of glucose-stimulated insulin secretion (GSIS). Furthermore, we showed that the remaining secretory activity required glucose uptake and metabolism because it can be blocked by inhibition of oxidative phosphorylation. Here, we extend these previous studies by analyzing, in GLUT2-null islets, glucose transporter isoforms and glucokinase expression and by measuring glucose usage, GSIS, and glucose-stimulated insulin mRNA biosynthesis. We show that in the absence of GLUT2, no compensatory expression of either GLUT1 or GLUT3 is observed and that glucokinase is expressed at normal levels. Glucose usage by isolated islets was increased between 1 and 6 mmol/l glucose but was not further increased between 6 and 20 mmol/l glucose. Parallel GSIS measurements showed that insulin secretion was not stimulated between 2.8 and 6 mmol/l glucose but was increased by &gt;4-fold between 6 and 20 mmol/l glucose. Stimulation by glucose of total protein and insulin biosynthesis was also markedly impaired in the absence of GLUT2. Finally, we re-expressed GLUT2 in GLUT2-null beta-cells using recombinant lentiviruses and demonstrated a restoration of normal GSIS. Together, these data show that in the absence of GLUT2, glucose can still be taken up by beta-cells, albeit at a low rate, and that this transport activity is unlikely to be attributed to GLUT1 or GLUT3. This uptake activity, however, is limiting for normal glucose utilization and signaling to secretion and translation. These data further demonstrate the key role of GLUT2 in murine beta-cells for glucose signaling to insulin secretion and biosynthesis.

Members of the PHO1 gene family show limited functional redundancy in phosphate transfer to the shoot, and are regulated by phosphate deficiency via distinct pathways.

The PHO1 family comprises 11 members in Arabidopsis thaliana. In order to decipher the role of these genes in inorganic phosphate (Pi) transport and homeostasis, complementation of the pho1 mutant, deficient in loading Pi to the root xylem, was determined by the expression of the PHO1 homologous genes under the control of the PHO1 promoter. Only PHO1 and the homologue PHO1;H1 could complement pho1. The PHO1;H1 promoter was active in the vascular cylinder of roots and shoots. Expression of PHO1;H1 was very low in Pi-sufficient plants, but was strongly induced under Pi-deficient conditions. T-DNA knock-out mutants of PHO1;H1 neither showed growth defects nor alteration in Pi transport dynamics, or Pi content, compared with wild type. However, the double mutant pho1/pho1;h1 showed a strong reduction in growth and in the capacity to transfer Pi from the root to the shoot compared with pho1. Grafting experiments revealed that phenotypes associated with the pho1 and pho1/pho1;h1 mutants were linked to the lack of gene expression in the root. The increased expression of PHO1;H1 under Pi deficiency was largely controlled by the transcription factor PHR1 and was suppressed by the phosphate analogue phosphite, whereas the increase of PHO1 expression was independent of PHR1 and was not influenced by phosphite. Together, these data reveal that although transfer of Pi to the root xylem vessel is primarily mediated by PHO1, the homologue PHO1;H1 also contributes to Pi loading to the xylem, and that the two corresponding genes are regulated by Pi deficiency by distinct signal transduction pathways.

Microtubule-associated protein 1B binds glyceraldehyde-3-phosphate dehydrogenase.

Microtubule-associated protein 1B, MAP1B, is a major cytoskeletal protein during brain development and one of the largest brain MAPs associated with microtubules and microfilaments. Here, we identified several proteins that bind to MAP1B via immunoprecipitation with a MAP1B-specific antibody, by one and two-dimensional gel electrophoresis and subsequent mass spectrometry identification of precipitated proteins. In addition to tubulin and actin, a variety of proteins were identified. Among these proteins were glyceraldehyde-3-phosphate dehydrogenase (GAPDH), heat shock protein 8, dihydropyrimidinase related proteins 2 and 3, protein-L-isoaspartate O-methyltransferase, beta-spectrin, and clathrin protein MKIAA0034, linking either directly or indirectly to MAP1B. In particular, GAPDH, a key glycolytic enzyme, was bound in large quantity to the heavy chain of MAP1B in adult brain tissue. In vitro binding studies confirmed a direct binding of GAPDH to MAP1B. In PC12 cells, GAPDH was found in cytoplasm and nuclei and partially co-localized with MAP1B. It disappeared from the cytoplasm under oxidative stress or after a disruption of cytoskeletal elements after colcemid or cytochalasin exposure. GAPDH may be essential in the local energy provision of cytoskeletal structures and MAP1B may help to keep this key enzyme close to the cytoskeleton.

Changes in insulin secretion and glucose metabolism induced by dexamethasone in lean and obese females

Résumé But: Chez les individus sveltes et en bonne santé, les modifications de la sensibilité à l'insuline secondaires à l'administration de dexaméthasone pendant deux jours sont compensées par une modification de la sécrétion d'insuline, permettant le maintien de l'homéostasie glucidique. Cette étude évalue les modifications du métabolisme glucidique et de la sécrétion d'insuline induites par une administration limitée de dexaméthasone chez les femmes obèses. Méthode de recherche: Onze femmes obèses ayant une tolérance au glucose normale ont été étudiées à deux reprises, 1° sans dexaméthasone et 2° après deux jours d'administration de dexaméthasone à faible dose. Un clamp hyperglycémique comportant deux plateaux (taux plasmatique de glucose à 7.5, respectivement 10 mM) avec du glucose marqué (6.6 ²H2 glc) a été utilisé pour déterminer la sécrétion d'insuline et le métabolisme du glucose du corps entier. Les résultats ont été comparés à ceux d'un groupe de huit femmes sveltes. Résultats : Sans dexaméthasone, les femmes obèses avaient un taux d'insuline plasmatique supérieur à jeun, durant le premier pic de sécrétion d'insuline, et aux deux plateaux hyperglycémiques. Elles avaient toutefois un métabolisme glucidique normal comparé à celui des femmes sveltes, ce qui indique une compensation adéquate. Après administration de la dexaméthasone, les femmes obèses avaient une augmentation du taux d'insuline plasmatique de 66 à 92%, mais une baisse de stockage du glucose de 15.4%. Ceci contrastait avec l'augmentation du taux d'insuline plasmatique de 91 à 113% chez les femmes sveltes et l'absence de changement de stockage du glucose du corps entier. Discussion : L'administration de dexaméthasone conduit à une baisse significative du stockage du glucose du corps entier pour une glycémie fixée chez les femmes obèses mais non chez les femmes sveltes. Ceci indique que les femmes obèses sont incapables d'accroître adéquatement leur sécrétion d'insuline. Abstract: Objective: In healthy lean individuals, changes in insulin sensitivity occurring as a consequence of a 2-day dexamethasone administration are compensated for by changes in insulin secretion, allowing glucose homeostasis to be maintained. This study evaluated the changes in glucose metabolism and insulin secretion induced by short-term dexamethasone administration in obese women. Research Methods and Procedures: Eleven obese women with normal glucose tolerance were studied on two occasions, without and after 2 days of low-dose dexamethasone administration. A two-step hyperglycemic clamp (7.5 and 10 mr1/1 glucose) with 6,6 2H2 glucose was used to assess insulin secretion and whole body glucose metabolism. Results were compared with those obtained in a group of eight lean women. Results: Without dexamethasone, obese women had higher plasma insulin concentrations in the fasting state, during the first phase of insulin secretion, and at the two hyperglycemic plateaus. However, they had normal whole body glucose metabolism compared with lean women, indicating adequate compensation. After dexamethasone, obese women had a 66% to 92% increase in plasma insulin concentrations but a 15.4% decrease in whole body glucose disposal. This contrasted with lean women, who had a 91% to 113% increase in plasma insulin concentrations, with no change in whole body glucose disposal. Discussion: Dexamethasone administration led to a significant reduction in whole body glucose disposal at fixed glycemia in obese but not lean women. This indicates that obese women are unable to increase their insulin secretion appropriately.