scholarly journals GLUCOSE METABOLISM OF THE SWIMBLADDER TISSUE OF THE EUROPEAN EEL ANGUILLA ANGUILLA

1993 ◽  
Vol 185 (1) ◽  
pp. 169-178 ◽  
Author(s):  
B. Pelster ◽  
P. Scheid
Keyword(s):  
Glucose Uptake ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Anguilla Anguilla ◽  
Pentose Phosphate ◽  
Co2 Production ◽  
European Eel ◽  
O2 Uptake ◽  
Lactate Release

Glucose uptake from, and lactate release into, the blood have been analysed in the active gas- depositing swimbladder of the immobilized European eel Anguilla anguilla. Under normoxic conditions, 0.72 micromole min-1 glucose was removed from the blood supply, while lactate was released into it at a rate of 1.16 micromole min-1. The rate of gas deposition into the swimbladder was significantly correlated with the rate of lactate production. Under hypoxic conditions, glucose consumption by, and lactate production of, the swimbladder tissue were reduced, as was the rate of gas deposition. Compared with normoxic conditions, lactate concentration in the swimbladder tissue was elevated after 1 h of hypoxia, indicating a decrease in lactate release. No difference in the osmolality of arterial and venous blood could be detected in these experiments. Combining the data for glucose uptake and lactate release measured under normoxic conditions with the values for O2 uptake and CO2 production of the swimbladder tissue measured under similar conditions in a previous study, a quantitative evaluation of glucose catabolism was performed. According to the O2 uptake of the tissue, only about 1 % of the glucose was oxidized, while about 80 % was fermented to lactic acid. The remaining 0.14 micromole min-1 glucose was presumably catabolized through the pentose phosphate shunt, as indicated by the CO2 production of 0.16 micromole min-1 that cannot be explained by aerobic metabolism.

scholarly journals Increased Pentose Phosphate Pathway Flux after Clinical Traumatic Brain Injury: A [1,2-13C2]glucose Labeling Study in Humans

2007 ◽  
Vol 27 (9) ◽  
pp. 1593-1602 ◽  
Author(s):  
Joshua R Dusick ◽  
Thomas C Glenn ◽  
WN Paul Lee ◽  
Paul M Vespa ◽  
Daniel F Kelly ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Jugular Bulb ◽  
Pentose Phosphate ◽  
Severe Tbi ◽  
The Difference ◽  
Gas Chromatography Mass Spectroscopy

Patients with traumatic brain injury (TBI) routinely exhibit cerebral glucose uptake in excess of that expected by the low levels of oxygen consumption and lactate production. This brings into question the metabolic fate of glucose. Prior studies have shown increased flux through the pentose phosphate cycle (PPC) during cellular stress. This study assessed the PPC after TBI in humans. [1,2-13C2]glucose was infused for 60 mins in six consented, severe-TBI patients (GCS < 9) and six control subjects. Arterial and jugular bulb blood sampled during infusion was analyzed for 13C-labeled isotopomers of lactate by gas chromatography/mass spectroscopy. The product of lactate concentration and fractional abundance of isotopomers was used to determine blood concentration of each isotopomer. The difference of jugular and arterial concentrations determined cerebral contribution. The formula PPC = ( m1/ m2)/(3 + ( m1/ m2)) was used to calculate PPC flux relative to glycolysis. There was enrichment of [1,2-13C2]glucose in arterial-venous blood (enrichment averaged 16.6% in TBI subjects and 28.2% in controls) and incorporation of 13C-label into lactate, showing metabolism of labeled substrate. The PPC was increased in TBI patients relative to controls (19.6 versus 6.9%, respectively; P = 0.002) and was excellent for distinguishing the groups (AUC = 0.944, P < 0.0001). No correlations were found between PPC and other clinical parameters, although PPC was highest in patients studied within 48 h of injury (averaging 33% versus 13% in others; P = 0.0006). This elevation in the PPC in the acute period after severe TBI likely represents a shunting of substrate into alternative biochemical pathways that may be critical for preventing secondary injury and initiating recovery.

scholarly journals Metabolism of the Perfused Swtmbladder of the European EEL: Oxygen, Carbon Dioxide, Glucose and Lactate Balance

1989 ◽  
Vol 144 (1) ◽  
pp. 495-506 ◽  
Author(s):  
B. PELSTER ◽  
H. KOBAYASHI ◽  
P. SCHEID
Keyword(s):  
Lactate Production ◽  
Anguilla Anguilla ◽  
Co2 Production ◽  
European Eel ◽  
Fick Principle ◽  
Partial Pressures ◽  
Gland Tissue ◽  
Arterial Inflow ◽  
Co2 Washout ◽  
Gas Gland

We have measured the metabolic activity in the vascularly isolated, salineperfused swimbladder of the eel (Anguilla anguilla) in order to investigate the pathways for CO2 formation in the gas gland tissue. Concentrations of O2, CO2, glucose and lactate were measured in the arterial inflow and venous outflow of the swimbladder, and metabolic rates were calculated by the direct Fick principle. 1. Total CO2 production, averaging 55.8nmol min−1, was about 4.6 times the O2 consumption (mean 12.0nmol min−1). This suggests that only about 22% of the CO2 is formed by aerobic glucose metabolism. 2. CO2 formation from HCO3− or CO2 washout does not appear to be significant in our experiments with steady perfusion of a saline containing a low level of HCO3−. 3. The ratio of lactate production to glucose uptake averaged 1.2, indicating that only 60% of the glucose is converted to lactate. Since only 1–2% of the glucose was found to be oxidized (2 nmol min−1), the extra glucose appears to be anoxidatively metabolized to CO2. 4. The anoxidative CO2 formation appears to be of functional importance for producing the high gas partial pressures of both CO2 and O2 which are required for secretion of these gases into the swimbladder.

Costal diaphragmatic O2 and lactate extraction in laryngeal hemiplegic ponies during exercise

1988 ◽  
Vol 65 (4) ◽  
pp. 1723-1728 ◽  
Author(s):  
M. Manohar ◽  
T. E. Goetz ◽  
D. Nganwa
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Hemoglobin Concentration ◽  
Insignificant Change ◽  
Resistive Breathing ◽  
O2 Extraction ◽  
Before And After ◽  
Arterial Po2

Diaphragmatic O2 and lactate extraction were examined in seven healthy ponies during maximal exercise (ME) carried out without, as well as with, inspiratory resistive breathing. Arterial and diaphragmatic venous blood were sampled simultaneously at rest and at 30-s intervals during the 4 min of ME. Experiments were carried out before and after left laryngeal hemiplegia (LH) was produced. During ME, normal ponies exhibited hypocapnia, hemoconcentration, and a decrease in arterial PO2 (PaO2) with insignificant change in O2 saturation. In LH ponies, PaO2 and O2 saturation decreased well below that in normal ponies, but because of higher hemoglobin concentration, arterial O2 content exceeded that in normal ponies. Because of their high PaCO2 during ME, acidosis was more pronounced in LH animals despite similar lactate values. Diaphragmatic venous PO2 and O2 saturation decreased with ME to 15.5 +/- 0.9 Torr and 18 +/- 0.5%, respectively, at 120 s of exercise in normal ponies. In LH ponies, corresponding values were significantly less: 12.4 +/- 1.3 Torr and 15.5 +/- 0.7% at 120 s and 9.8 +/- 1.4 Torr and 14.3 +/- 0.6% at 240 s of ME. Mean phrenic O2 extraction plateaued at 81 and 83% in normal and LH animals, respectively. Significant differences in lactate concentration between arterial and phrenic-venous blood were not observed during ME. It is concluded that PO2 and O2 saturation in the phrenic-venous blood of normal ponies do not reach their lowest possible values even during ME. Also, the healthy equine diaphragm, even with the added stress of inspiratory resistive breathing, did not engage in net lactate production.

Glucose and oxygen metabolism in the fetal foal during late gestation

1995 ◽  
Vol 269 (6) ◽  
pp. R1455-R1461 ◽  
Author(s):  
A. L. Fowden ◽  
M. Silver
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Oxygen Metabolism ◽  
Endogenous Glucose Production ◽  
Late Gestation ◽  
Co2 Production ◽  
O2 Uptake ◽  
Fed State ◽  
Glucose Carbon ◽  
Lactate Uptake

With the use of [U-14C]glucose tracer methodology, the rates of umbilical uptake, utilization, oxidation, and production of glucose were determined in nine chronically catheterized fetal foals in the fed state between 268 and 325 days of gestation (term approximately 335 days). At the same time, the rates of umbilical O2 and lactate uptake were measured in all nine fetuses by Fick principle. The mean fetal rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon were 36.9 +/- 2.5, 36.4 +/- 1.7, and 117.7 +/- 17.4 mumol.min-1.kg fetal body wt-1, respectively (n = 9). Endogenous glucose production was therefore negligible in the fetal foal in the fed state. Production of CO2 from glucose carbon accounted for 40.9 +/- 6.5% of the umbilical O2 uptake, which averaged 292 +/- 15 mumol.min-1.kg-1 (n = 9). No significant changes in fetal glucose or O2 metabolism were observed with increasing gestational age. The rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon (P < 0.01), but not the rate of umbilical O2 uptake (P > 0.05), were positively correlated with the fetal blood glucose level. There was a significant umbilical lactate uptake in the fetuses older than 290 days (12.3 +/- 4.1 mumol.min-1.kg-1, n = 5, P < 0.05) but not in the younger animals (6.2 +/- 9.6 mumol.min-1.kg-1, n = 4, P > 0.05). Hence, glucose is used for both oxidative and nonoxidative metabolism in utero and is a major, although not the sole, oxidative substrate in the fetal foal during late gestation.

scholarly journals Down regulating PHGDH affects the lactate production of Sertoli cells in varicocele

2020 ◽  
Author(s):  
Wen-bin Guo ◽  
Zhen-hui Huang ◽  
Cheng Yang ◽  
Xian-yuan Lv ◽  
Hui Xia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Male Infertility ◽  
Western Blot ◽  
Sertoli Cells ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Down Regulation ◽  
Regulation Model

Abstract Background: Although varicocele is considered to be one of the leading causes of male infertility, the precise mechanism underlying how varicocele leads to male infertility is not completely understood. We found the lactate concentration on the varicocele side of the patients was decreased compare with peripheral venous blood. In the testicles, the lactate produced by the sertoli cells (TM4) through the glycolysis pathway provides most of the energy needed for spermatogenesis, the reduction of lactate will affect spermatogenesis. The objective of this study was to investigate the mechanism of this abnormal energy metabolism phenomenon in varicocele.Methods: In this study, we collected the testicular tissue from patients with varicocele, the glycolysis related proteins PHGDH was identified by iTRAQ proteomics technology. Experimental rat varicocele model was constructed according to our new clip technique, the mRNA and protein expression levels of PHGDH were examined with qRT-PCR and Western blotting. We constructed a TM4 cell of PHGDH down-regulation model, and then detected the glucose consumption, LDH activities and lactate production in the TM4 cells. Western blot was conducted to investigate the effects of PHGDH on the expression of phosphoserine phosphatase (PSPH) and Pyruvate kinase M2 (PKM2). Flow cytometry was used to detect the cell apoptosis and cell cycle in TM4 cells.Results: The results showed that testicular protein PHGDH was down-regulated in varicocele. Down-regulation of PHGDH in TM4 cells significantly decreased the glucose consumption, LDH activities and lactate production in the TM4 cells, indicating that the low expression of PHGDH ultimately led to a decrease in lactate production by affecting the glycolysis. The Western blot results showed that the down-regulation of PHGDH significantly reduced the expression of pathway protein PSPH and PKM2, leading to the reduction of lactate production. Moreover, PHGDH knockdown can promote apoptosis and inhibit cell cycle to affect cell growth.Conclusions: Overall, we conformed that varicocele lead to the decreasing of testis lactate production. Down-regulation of PHGDH in TM4 cells may mediate the process of abnormal glucose metabolism. Our study provide new insight into the mechanisms underlying metabolism-associated male infertility and suggests a novel therapeutic target for male infertility.

Activities of Enzymes for Glucose Catabolism in the Swimbladder of the European Eel Anguilla Anguilla

1991 ◽  
Vol 156 (1) ◽  
pp. 207-213 ◽  
Author(s):  
BERND PELSTER ◽  
PETER SCHEID
Keyword(s):  
White Muscle ◽  
Anguilla Anguilla ◽  
Great Depth ◽  
Pentose Phosphate ◽  
European Eel ◽  
Glucose Catabolism ◽  
Rete Mirabile ◽  
Special Adaptation ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Pentose Phosphate Shunt

Gas secretion into the swimbladder of the eel relies on the production of CO2 and lactic acid from glucose in the swimbladder epithelium. The activities of the enzymes involved in glucose catabolism have been measured and compared with those in the rete mirabile, the liver and white skeletal muscle to evaluate whether the pentose phosphate shunt may contribute to glucose metabolism in the swimbladder tissue. The activities of enzymes of the pentose phosphate shunt were higher in the swimbladder epithelium than in white muscle, and close to those in the liver. The activities of the enzymes of anaerobic glycolysis were 2–5 times higher in the swimbladder epithelium than in the rete mirabile, reaching or even exceeding the levels in liver and white muscle, whereas the activities of the enzymes of oxidative metabolism were extremely low. Compared to enzymes of the other tissues, swimbladder phosphofructokinase and glucose-6-phosphate dehydrogenase showed no special adaptation to low pH values. The results show that the swimbladder epithelium is equipped with enzymes that produce CO2 from glucose without the removal of O2, which is particularly advantageous for creating the high gas partial pressures needed for filling the swimbladder at great depth.

Effects of priming exercise on VO2 kinetics and O2 deficit at the onset of stepping and cycling

1989 ◽  
Vol 66 (5) ◽  
pp. 2023-2031 ◽  
Author(s):  
P. E. di Prampero ◽  
P. B. Mahler ◽  
D. Giezendanner ◽  
P. Cerretelli
Keyword(s):  
Lactate Concentration ◽  
Lactate Production ◽  
Blood Lactate Concentration ◽  
Work Load ◽  
O2 Uptake ◽  
Vo2 Max ◽  
Double Exponential ◽  
Vo2 Kinetics ◽  
Male Subjects ◽  
O2 Deficit

Breath-by-breath O2 uptake (VO2) kinetics and increase of blood lactate concentration (delta Lab) were determined at the onset of square-wave stepping (S) or cycling (C) exercise on six male subjects during 1) transition from rest (R) to constant work load, 2) transition from lower to heavier work loads, wherein the baseline VO2 (VO2 s) was randomly chosen between 20 and 65% of the subjects' maximal O2 uptake (VO2 max), and 3) inverse transition from higher to lower work loads and/or to rest. VO2 differences between starting and arriving levels were 20–60% VO2 max. In C, the VO2 on-response became monotonically slower with increasing VO2 s, the half time (t1/2) increasing from approximately 22 s for VO2 s = R to approximately 63 s when VO2 s approximately equal to 50% VO2 max. In S, the fastest VO2 kinetics (t1/2 = 16 s) was attained from VO2 s = 15–30% VO2 max, the t1/2 being approximately 25 s when starting from R or from 50% VO2 max. The slower VO2 kinetics in C were associated with a much larger delta Lab. The VO2 kinetics in recovery were essentially the same in all cases and could be approximated by a double exponential with t1/2 of 21.3 +/- 6 and 93 +/- 45 s for the fast and slow components, respectively. It is concluded that the O2 deficit incurred is the sum of three terms: 1) O2 stores depletion, 2) O2 equivalent of early lactate production, and 3) O2 equivalent of phosphocreatine breakdown.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Inhibition of glucose uptake and glycogenolysis by availability of oleate in well-oxygenated perfused skeletal muscle

1977 ◽  
Vol 168 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Michael J. Rennie ◽  
John O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Glucose Uptake ◽  
Contractile Activity ◽  
Haemoglobin Concentration ◽  
Lactate Production ◽  
O2 Uptake ◽  
Perfusion Medium ◽  
Red Muscle ◽  
Intracellular Glucose

The effects of exogenous oleate on glucose uptake, lactate production and glycogen concentration in resting and contracting skeletal muscle were studied in the perfused rat hindquarter. In preliminary studies with aged erythrocytes at a haemoglobin concentration of 8g/100ml in the perfusion medium, 1.8mm-oleate had no effect on glucose uptake or lactate production. During these studies it became evident that O2 delivery was inadequate with aged erythrocytes. Perfusion with rejuvenated human erythrocytes at a haemoglobin concentration of 12g/100ml resulted in a 2-fold higher O2 uptake at rest and a 4-fold higher O2 uptake during muscle contraction than was obtained with aged erythrocytes. Rejuvenated erythrocytes were therefore used in subsequent experiments. Glucose uptake and lactate production by the well-oxygenated hindquarter were inhibited by one-third, both at rest and during muscle contraction, when 1.8mm-oleate was added to the perfusion medium. Addition of oleate also significantly protected against glycogen depletion in the fast-twitch red and slow-twitch red types of muscle, but not in white muscle, during sciatic-nerve stimulation. In the absence of added oleate, glucose was confined to the extracellular space in resting muscle. Addition of oleate resulted in intracellular glucose accumulation in red muscle. Contractile activity resulted in accumulation of intracellular glucose in all three muscle types, and this effect was significantly augmented in the red types of muscle by perfusion with oleate. The concentrations of citrate and glucose 6-phosphate were also increased in red muscle perfused with oleate. We conclude that, as in the heart, availability of fatty acids has an inhibitory effect on glucose uptake and glycogen utilization in well-oxygenated red skeletal muscle.

Retinal glucose metabolism in mice lacking the L-glutamate/aspartate transporter

2004 ◽  
Vol 21 (4) ◽  
pp. 637-643 ◽  
Author(s):  
VIJAY P. SARTHY ◽  
V. JOSEPH DUDLEY ◽  
KOHICHI TANAKA
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glial Cells ◽  
Glutamate Transporter ◽  
Lactate Production ◽  
Müller Cells ◽  
Mouse Retina ◽  
Muller Cells ◽  
Wild Type ◽  
Lactate Release

The conventional view that glucose is the substrate for neuronal energy metabolism has been recently challenged by the “lactate shuttle” hypothesis in which glutamate cycling in glial cells drives all neuronal glucose metabolism. According to this view, glutamate released by activated retinal neurons is transported into Müller (glial) cells where it triggers glycolysis. The lactate released by Müller cells serves as the energy substrate for neuronal metabolism. Because the L-Glutamate/aspartate transporter (GLAST) is the predominant, Na+-dependent, glutamate transporter expressed by Müller cells, we have used GLAST-knockout (GLAST−/−) mice to examine the relationship between lactate release and GLAST activity in the retina. We found that glucose uptake and lactate production by the GLAST−/− mouse retina was similar to that observed in the wild type mouse retina. Furthermore, addition of 1 mM glutamate and NH4Cl to the incubation medium did not further stimulate glucose uptake in either case. When lactate release was measured in the presence of the lactate uptake inhibitor, α-cyano-4-hydroxycinnamate, there was no significant change in the amount of lactate released by retinas from GLAST−/− mice compared to the wild type. Finally, lactate release was similar under both dark and light conditions. These results show that lactate production and release is not altered in retinas of GLAST−/− mice, which suggests that metabolic coupling between photoreceptors and Müller cells is not mediated by the glial glutamate transporter, GLAST.

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