Lactate formation in Callianassa californiensis and Upogebia pugettensis (Crustacea: Thalassinidea)

1979 ◽  
Vol 50 (3) ◽  
pp. 249-253 ◽  
Author(s):  
A. W. Pritchard ◽  
S. Eddy

2014 ◽  
Vol 13 (1) ◽  
pp. 78 ◽  
Author(s):  
Dandan Niu ◽  
Kangming Tian ◽  
Bernard A Prior ◽  
Min Wang ◽  
Zhengxiang Wang ◽  
...  


2005 ◽  
Vol 9 (5) ◽  
pp. 599-607 ◽  
Author(s):  
Navinchandra Asthana ◽  
Aspi Kolah ◽  
Dung T. Vu ◽  
Carl T. Lira ◽  
Dennis J. Miller


Author(s):  
Luisa Fasulo ◽  
Barbara Fulgosi ◽  
Sebastiano Colombatto ◽  
Maria Angelica Grillo


1998 ◽  
Vol 85 (2) ◽  
pp. 627-634 ◽  
Author(s):  
Russell S. Richardson ◽  
Elizabeth A. Noyszewski ◽  
John S. Leigh ◽  
Peter D. Wagner

It remains controversial whether lactate formation during progressive dynamic exercise from submaximal to maximal effort is due to muscle hypoxia. To study this question, we used direct measures of arterial and femoral venous lactate concentration, a thermodilution blood flow technique, phosphorus magnetic resonance spectroscopy (MRS), and myoglobin (Mb) saturation measured by 1H nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate efflux from the muscle and intracellular[Formula: see text] with subjects breathing room air and 12% O2. Data were obtained at 50, 75, 90, and 100% of quadriceps maximal O2 consumption at each fraction of inspired O2. Mb saturation was significantly lower in hypoxia than in normoxia [40 ± 3 vs. 49 ± 3% (SE)] throughout incremental exercise to maximal work rate. With the assumption of a[Formula: see text] at which 50% of Mb-binding sites are bound with O2 of 3.2 Torr, Mb-associated [Formula: see text] averaged 3.1 ± 0.3 and 2.3 ± 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular[Formula: see text] across the range of incremental exercise to maximum ( r = 0.03 and 0.07 in normoxia and hypoxia, respectively) but linearly related to O2 consumption ( r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope in 12% O2. Net lactate efflux was also linearly related to intracellular pH ( r = 0.94 and 0.98 in normoxia and hypoxia, respectively). These data suggest that with increasing work rate, at a given fraction of inspired O2, lactate efflux is unrelated to muscle cytoplasmic [Formula: see text], yet the efflux is higher in hypoxia. Catecholamine values from comparable studies are included and indicate that lactate efflux in hypoxia may be due to systemic rather than intracellular hypoxia.



1990 ◽  
Vol 259 (3) ◽  
pp. C455-C461 ◽  
Author(s):  
M. J. Tang ◽  
R. L. Tannen

Primary cultures of rabbit proximal tubules, which revert to a glycolytic profile as reflected by increased activity of pyruvate kinase (PK) paralleled by increased glucose consumption and lactate formation, were utilized to explore the relationship between glycolytic metabolism and proliferation. Tubules placed in serum-free, hormonally defined Dulbecco's modified Eagle's medium with 5 mM glucose exhibited logarithmic growth beginning on day 3 in culture. The increase in PK activity lagged approximately 1 day behind, suggesting that the reversion to glycolysis is a consequence of rather than a prerequisite for cellular proliferation. Tubules cultured in 0.5 mM as contrasted with 25 mM glucose exhibited heightened proliferation reflected by an increase in protein content and cell number on day 5 in culture. The heightened proliferation was accompanied by increased PK activity. On day 9, after confluency had been achieved, no differences in protein content or PK activity were detected between tubules cultured in different glucose concentrations. These findings indicate that a low glucose concentration is mitogenic for renal proximal tubules and that the proliferative process in some fashion up-regulates the activity of the glycolytic enzyme PK. Furthermore, because accelerated growth proceeds in the presence of glucose restriction, the energy from glycolysis is not required for the proliferative process.



1973 ◽  
Vol 134 (3) ◽  
pp. 697-705 ◽  
Author(s):  
Hans A. Krebs ◽  
Reginald Hems ◽  
Patricia Lund

1. The rate of gluconeogenesis from alanine in the perfused rat liver is affected by the presence of other metabolizable substances, especially fatty acids, ornithine and ethanol. Gluconeogenesis is accelerated by oleate and by ornithine. When both oleate and ornithine were present the acceleration was greater than expected on the basis of mere additive effects. 2. Much NH3 and some urea were formed from alanine when no ornithine was added. With ornithine almost all the nitrogen released from alanine appeared as urea. 3. Lactate was a major product of alanine metabolism. Addition of oleate, and especially of oleate plus ornithine, decreased lactate formation. 4. Ethanol had no major effect on gluconeogenesis from alanine when this was the sole added precursor. Gluconeogenesis was strongly inhibited (87%) when oleate was also added, but ethanol greatly accelerated gluconeogenesis when ornithine was added together with alanine. 5. In the absence of ethanol the alanine carbon and alanine nitrogen removed were essentially recovered in the form of glucose, lactate, pyruvate, NH3 and urea. 6. In the presence of ethanol the balance of both alanine carbon and alanine nitrogen showed substantial deficits. These deficits were largely accounted for by the formation of aspartate and glutamine, the formation of which was increased two- to three-fold. 7. When alanine was replaced by lactate plus NH4Cl, ethanol also caused a major accumulation of amino acids, especially of aspartate and alanine. 8. Earlier apparently discrepant results on the effects of ethanol on gluconeogenesis from alanine are explained by the fact that under well defined conditions ethanol can inhibit, or accelerate, or be without major effect on the rate of gluconeogenesis. 9. It is pointed out that in the synthesis of urea through the ornithine cycle half of the nitrogen must be supplied in the form of asparate and half in the form of carbamoyl phosphate. The accumulation of aspartate and other amino acids suggests that ethanol interferes with the control mechanisms which regulate the stoicheiometric formation of aspartate and carbamoyl phosphate.



1973 ◽  
Vol 134 (4) ◽  
pp. 899-906 ◽  
Author(s):  
Keith Snell ◽  
Deryck G. Walker

1. The concentrations of liver glycogen and plasma d-glucose were measured in caesarian-delivered newborn rats at time-intervals up to 3h after delivery after treatment of the neonatal rats with glucagon, dibutyryl cyclic AMP, cortisol or cortisol+dibutyryl cyclic AMP. Glycogenolysis was promoted by glucagon or dibutyryl cyclic AMP in the third hour after birth but not at earlier times. Cortisol and dibutyryl cyclic AMP together (but neither agent alone) promoted glycogenolysis in the second hour after birth, but no hormone combination was effective in the first postnatal hour. 2. The specific radioactivity of plasma d-glucose was measured as a function of time for up to 75 min after the intraperitoneal injection of d-[6-14C]glucose and d-[6-3H]glucose into newborn rats at delivery and after treatment with glucagon or actinomycin D. Glucagon-mediated hyperglycaemia at this time was due to an increased rate of glucose formation and a decreased rate of glucose utilization. Actinomycin D prevented glucose formation and accelerated the rate of postnatal hypoglycaemia. 3. The specific radioactivity of plasma l-lactate and the incorporation of 14C into plasma d-glucose was measured as a function of time after the intraperitoneal injection of l-[U-14C]lactate into glucagon- or actinomycin D-treated rats immediately after delivery. The calculated rates of lactate formation were unchanged by either treatment, but lactate utilization was stimulated by glucagon administration. Glucagon stimulated and actinomycin D diminished 14C incorporation into plasma d-glucose. 4. The factors involved in the initiation of glycogenolysis and gluconeogenesis in the rat immediately after birth are discussed.



Author(s):  
T Mann

Background. Lactate or, as it was customarily known, ‘lactic acid’ was one of the first molecules to attract the attention of early exercise scientists, mainly because blood lactate concentration could be measured and was shown to increase with increasing exercise intensity. This connection resulted in lactate being associated with numerous other events associated with high-intensity exercise including muscle cramps, fatigue, acidosis and post-exercise muscle soreness. Nobel prize-winning research by AV Hill and Otto Meyerhof provided a rational explanation linking lactate to anaerobiosis and acidosis, which resulted in this relationship being widely accepted as fact. It was only following isotopic tracer studies of George Brooks and others that the true role of lactate during rest and exercise was revealed. Conclusions. Lactate is now acknowledged as an important intermediate of carbohydrate metabolism, taken up from the blood by tissues such as skeletal and cardiac muscle as a substrate for oxidation. Furthermore, lactate formation consumes a proton, thereby buffering against muscle acidosis. For this reason, lactate production forms an essential aid to endurance performance rather than a hindrance.



1987 ◽  
Vol 133 (1) ◽  
pp. 339-352
Author(s):  
S. MORRIS ◽  
C.R. BRIDGES ◽  
M. K. GRIESHABER

The binding of Ca2+ to the haemocyanin of the crayfish Austropotamobius pallipes was investigated. The amount of bound Ca2+ was determined using an ultrafiltration technique to produce haemocyanin-free solutions, the Ca2+ concentration of which could then be compared with that of the original, unfiltered solution. Any difference between the two values would indicate the amount of calcium bound by haemocyanin. The effect of L-lactate on Ca2+ binding was investigated by determining the amount of bound ion at different concentrations of L-lactate. In addition, oxygen equilibrium curves were constructed for some of the solutions to verify that the haemocyanin oxygen affinity remained sensitive to L-lactate and to determine whether the haemocyanin was functionally similar to that used in previous investigations. With 17 mmol 1−1 total Ca2+ and approximately 1 mmol 1−1 L-lactate the number of Ca2+ binding sites was estimated to be between eight and nine per haemocyanin molecule. Without taking into account the formation of calcium lactate, the observed dependency of Ca2+-haemocyanin binding on L-lactate concentration could best be described by the equation: Ca2+/Hc = 8.64-0.32[lactate−]. A ‘worst case’ estimate for maximum calcium lactate formation, assuming Ca2+ to be the only counterion available to lactate, altered the relationship slightly to: Ca2+/Hc = 8.65-0.35[lactate−]. Note: Present address: Department of Biological Sciences, University of Calgary, 2500 University Drive N/V, Calgary, Alberta, Canada T2N 1N4.



2020 ◽  
pp. 1-8
Author(s):  
Yunfeng Zhao ◽  
Cherie Ann Nathan ◽  
Chunjing Zhang ◽  
Hongyan Du ◽  
Manikandan Panchatcharam ◽  
...  

Background: New adjuvant therapies for human head and neck (H&N) cancer to improve the quality of life of the patients are in great demand. Our early studies have demonstrated that uncoupling protein 2 (UCP2) is upregulated in the tumor tissues of H&N cancer compared to the adjacent normal tissues; however, the role of UCP2 in H&N cancer has not been studied. Objective: In this manuscript, we aim to examine whether UCP2 contributes to H&N cancer progression in vitro. Methods: We generated UCP2 stable knockdown H&N cancer cells and detected the effects of UCP2 inhibition on cell proliferation, migration, invasion, 3D spheroid formation, and the sensitivity to a chemodrug treatment. Results: Knockdown of UCP2 suppressed the progression of H&N cancer in vitro, which might be mediated via the following mechanism: 1) increased the G1 phase whereas decreased the S phase of the cell cycle, which could be mediated by suppression of the G1/S regulators including CDK4/6 and cyclin D1. 2) Decreased mitochondrial oxygen consumption, ATP production, and lactate formation, which is consistent with the downregulation of c-Myc. 3) FAK may serve as the upstream signaling molecule, and its action was mediated by Akt and ERK. Conclusions: Our studies first demonstrate that targeting UCP2 may suppress H&N cancer progression in vitro.



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