scholarly journals Faculty Opinions recommendation of Efferocytosis induces a novel SLC program to promote glucose uptake and lactate release.

2021 ◽  
Author(s):  
Sekhar Reddy
Keyword(s):  
Glucose Uptake ◽  
Lactate Release

Metabolic fate of glucose in reversible low-flow ischemia of the isolated working rat heart

1996 ◽  
Vol 270 (3) ◽  
pp. H817-H826 ◽  
Author(s):  
H. Bolukoglu ◽  
G. W. Goodwin ◽  
P. H. Guthrie ◽  
S. G. Carmical ◽  
T. M. Chen ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Glycogen Synthesis ◽  
Coronary Perfusion Pressure ◽  
Low Flow ◽  
Coronary Perfusion ◽  
Myocardial Glucose Metabolism ◽  
Lactate Release ◽  
Exogenous Substrate ◽  
Rat Hearts

The acute adaptation of myocardial glucose metabolism in response to low-flow ischemia and reperfusion was investigated in isolated working rat hearts perfused with bicarbonate saline containing glucose (10 mM) and insulin (40 microU/ml). Reversible low-flow ischemia was induced by reducing coronary perfusion pressure from 100 to 35 cmH2O. Tritiated glucose was used to assess rates of glucose transport and phosphorylation, flux from glucose to pyruvate, and oxidation of exogenous glucose. Rates of glycogen synthesis and glycolysis were also assessed. With ischemia, cardiac power decreased by more than two-thirds. Rates of glucose uptake and flux from glucose to pyruvate remained unchanged, while glucose oxidation declined by 61%. Rates of lactate release more than doubled, and fractional enrichment of glycogen remained the same. During reperfusion, glucose oxidation returned to the preischemic values. When isoproterenol was added during ischemia, glucose uptake increased, glycogen decreased, and lactate release increased. No effect was seen with pacing. We conclude that during low-flow ischemia and with glucose as the only exogenous substrate, net glucose uptake remains unchanged. There is a reversible redirection between glycolysis and glucose oxidation, while glycogen synthesis continues during ischemia and is enhanced with reperfusion.

Effect of fast duration on disposition of an intraduodenal glucose load in the conscious dog

1999 ◽  
Vol 276 (3) ◽  
pp. E543-E552 ◽  
Author(s):  
Pietro Galassetti ◽  
Katherine S. Hamilton ◽  
Fiona K. Gibbons ◽  
Deanna P. Bracy ◽  
Drury B. Lacy ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Prolonged Fasting ◽  
Glucose Administration ◽  
Lactate Release ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Arterial Insulin ◽  
Arterial Glucose

The effects of prior fast duration (18 h, n = 8; 42 h, n = 8) on the glycemic and tissue-specific responses to an intraduodenal glucose load were studied in chronically catheterized conscious dogs. [3-3H]glucose was infused throughout the study. After basal measurements, glucose spiked with [U-14C]glucose was infused for 150 min intraduodenally. Arterial insulin and glucagon were similar in the two groups. Arterial glucose (mg/dl) rose ∼70% more during glucose infusion after 42 h than after an 18-h fast. The net hepatic glucose balance (mg ⋅ kg−1⋅ min−1) was similar in the two groups (basal: 1.8 ± 0.2 and 2.0 ± 0.3; glucose infusion: −2.2 ± 0.5 and −2.2 ± 0.7). The intrahepatic fate of glucose was 79% glycogen, 13% oxidized, and 8% lactate release after a 42-h fast; it was 23% glycogen, 21% oxidized, and 56% lactate release after an 18-h fast. Net hindlimb glucose uptake was similar between groups. The appearance of intraduodenal glucose during glucose infusion (mg/kg) was 900 ± 50 and 1,120 ± 40 after 18- and 42-h fasts ( P < 0.01). Conclusion: glucose administration after prolonged fasting induces higher circulating glucose than a shorter fast (increased appearance of intraduodenal glucose); liver and hindlimb glucose uptakes and the hormonal response, however, are unchanged; finally, an intrahepatic redistribution of carbons favors glycogen deposition.

Nutritive blood flow improves interstitial glucose and lactate exchange in perfused rat hindlimb

2002 ◽  
Vol 283 (1) ◽  
pp. H186-H192 ◽  
Author(s):  
John M. B. Newman ◽  
Stephen Rattigan ◽  
Michael G. Clark
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Oxygen Uptake ◽  
Glucose Uptake ◽  
Ang Ii ◽  
Constant Flow ◽  
Lactate Release ◽  
Interstitial Concentration ◽  
Interstitial Glucose ◽  
Lactate Exchange

Microdialysis was used to assess the interstitial concentrations of glucose and lactate in the constant-flow-perfused rat hindlimb under varying levels of nutritive flow controlled by vasoconstrictors. Increased nutritive flow was achieved by norepinephrine (NE) or angiotensin II (ANG II) and decreased nutritive flow by serotonin (5-HT). NE and ANG II increased oxygen and glucose uptake as well as hindlimb lactate release by 50%. 5-HT decreased oxygen uptake by 15% but had no significant effect on glucose uptake or hindlimb lactate release. Microdialysis recovery of glucose and lactate was significantly elevated by NE and ANG II and decreased by 5-HT. The calculated interstitial concentration of glucose was increased by NE and ANG II but decreased by 5-HT. The interstitial concentration of lactate was decreased by NE and ANG II but increased by 5-HT. In all cases, nitroprusside reversed the effects of the vasoconstrictors. These data indicate that increased nutritive blood flow enhances the exchange of glucose and lactate by improving the supply of glucose to and the removal of lactate from the interstitium.

Fructose augments infection-impaired net hepatic glucose uptake during TPN administration

2001 ◽  
Vol 280 (5) ◽  
pp. E703-E711 ◽  
Author(s):  
Christine M. Donmoyer ◽  
Joseph Ejiofor ◽  
D. Brooks Lacy ◽  
Sheng-Song Chen ◽  
Owen P. McGuinness
Keyword(s):  
Glucose Uptake ◽  
Vena Cava ◽  
Fibrin Clot ◽  
Glycogen Storage ◽  
Glucose Disposal ◽  
Lactate Release ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Arteriovenous Difference

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) and net hepatic lactate release (NHLR) are markedly reduced (↓∼45 and ∼65%, respectively) with infection. Because small quantities of fructose are known to augment hepatic glucose uptake and lactate release in normal fasted animals, the aim of this work was to determine whether acute fructose infusion with TPN could correct the impairments in NHGU and NHLR during infection. Chronically catheterized conscious dogs received TPN for 5 days via the inferior vena cava at a rate designed to match daily basal energy requirements. On the third day of TPN administration, a sterile (SHAM, n = 12) or Escherichia coli-containing (INF, n = 11) fibrin clot was implanted in the peritoneal cavity. Forty-two hours later, somatostatin was infused with intraportal replacement of insulin (12 ± 2 vs. 24 ± 2 μU/ml, SHAM vs. INF, respectively) and glucagon (24 ± 4 vs. 92 ± 5 pg/ml) to match concentrations previously observed in sham and infected animals. After a 120-min basal period, animals received either saline (Sham+S, n = 6; Inf+S, n = 6) or intraportal fructose (0.7 mg · kg−1· min−1; Sham+F, n = 6; Inf+F, n = 5) infusion for 180 min. Isoglycemia of 120 mg/dl was maintained with a variable glucose infusion. Combined tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism. Acute fructose infusion with TPN augmented NHGU by 2.9 ± 0.4 and 2.5 ± 0.3 mg · kg−1· min−1in Sham+F and Inf+F, respectively. The majority of liver glucose uptake was stored as glycogen, and NHLR did not increase substantially. Therefore, despite an infection-induced impairment in NHGU and different hormonal environments, small amounts of fructose enhanced NHGU similarly in sham and infected animals. Glycogen storage, not lactate release, was the preferential fate of the fructose-induced increase in hepatic glucose disposal in animals adapted to TPN.

Characteristics of rat hindlimbs perfused with erythrocyte- and albumin-free medium

1986 ◽  
Vol 251 (1) ◽  
pp. C78-C84 ◽  
Author(s):  
M. Shiota ◽  
T. Sugano
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Flow Rate ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Integral Function ◽  
Maximal Effect ◽  
Free Medium ◽  
Bicarbonate Buffer ◽  
Lactate Release

The isolated rat hindlimb was perfused with Krebs-bicarbonate buffer without erythrocytes and albumin in a flow-through mode at 32 degrees C, and the viability and metabolic characteristics of perfused skeletal muscle were examined. 1) With the flow rate at 15 ml X min-1 X leg-1, glucose and O2 uptake, lactate release, lactate-to-pyruvate ratio in effluent, and tissue creatine phosphate and adenine nucleotides remained constant at rest during perfusion for 90 min. The twitch tension changed little over perfusion. 2) When the leg was stimulated at a frequency below 0.5 Hz, the standard flow rate adequately delivered O2 to the perfused leg. Sciatic nerve stimulation enhanced glucose uptake in the absence of insulin. 3) The stimulatory effect of insulin on glucose uptake was observed with a concentration as low as 0.1 mU/ml, and maximal effect was at approximately mU/ml, with a nearly eightfold increase in glucose uptake. 4) Epinephrine and isoproterenol at a concentration of 0.5 nM stimulated lactate release, with maximal effect at 5 nM. The response to catecholamines was reversible and reproducible with a single preparation during the perfusion period of 120 min. The results indicated that the perfusion of hindlimb with a hemoglobin- and albumin-free medium is a convenient and reliable tool for the biochemical investigations of the integral function of hindlimb skeletal muscle.

scholarly journals Effect of acetoacetate on glucose metabolism in the soleus and extensor digitorum longus muscles of the rat

1977 ◽  
Vol 162 (3) ◽  
pp. 557-568 ◽  
Author(s):  
E Z Maizels ◽  
N B Ruderman ◽  
M N Goodman ◽  
D Lau
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Extensor Digitorum Longus ◽  
Similar Rate ◽  
Extensor Digitorum ◽  
Lactate Release ◽  
Red Muscle ◽  
Slow Twitch ◽  
Fast Twitch

1. The effect of acetoacetate on glucose metabolism was compared in the soleus, a slow-twitch red muscle, and the extensor digitorum longus, a muscle composed of 50% fast-twitch red and 50% white fibres. 2. When incubated for 2h in a medium containing 5 mM-glucose and 0.1 unit of insulin/ml, rates of glucose uptake, lactate release and glucose oxidation in the soleus were 19.6, 18.6 and 1.47 micronmol/h per g respectively. Acetoacetate (1.7 mM) diminished all three rates by 25-50%; however, it increased glucose conversion into glycogen. In addition, it caused increases in tissue glucose, glucose 6-phosphate and fructose 6-phosphate, suggesting inhibition of phosphofructokinase. The concentrations of citrate, an inhibitor of phosphofructokinase, and of malate were also increased. 3. Rates of glucose uptake and lactate release in the extensor digitorum longus were 50-80% of those in the soleus. Acetoacetate caused moderate increases in tissue glucose 6-phosphate and possibly citrate, but it did not decrease glucose uptake or lactate release. 4. The rate of glycolysis in the soleus was approximately five times that previously observed in the perfused rat hindquarter, a muscle preparation in which acetoacetate inhibits glucose oxidation, but does not alter glucose uptake or glycolysis. A similar rate of glycolysis was observed when the soleus was incubated with a glucose-free medium. Under these conditions, tissue malate and the lactate/pyruvate ratio in the medium were decreased, and acetoacetate did not decrease lactate release or increase tissue citrate or glucose 6-phosphate. An intermediate rate of glycolysis, which was not decreased by acetoacetate, was observed when the soleus was incubated with glucose, but not insulin. 5. The data suggest that acetoacetate glucose inhibits uptake and glycolysis in red muscle under conditions that resemble mild to moderate exercise. They also suggest that the accumulation of citrate in these circumstances is linked to the rate of glycolysis, possibly through the generation of cytosolic NADH and malate formation.

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 Glucose metabolism in perfused skeletal muscle. Effects of starvation, diabetes, fatty acids, acetoacetate, insulin and exercise on glucose uptake and disposition

1976 ◽  
Vol 158 (2) ◽  
pp. 191-202 ◽  
Author(s):  
M Berger ◽  
S A Hagg ◽  
M N Goodman ◽  
N B Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Lactate Oxidation ◽  
Fed State ◽  
Lactate Release ◽  
Sciatic Nerve Stimulation

1. The regulation of glucose uptake and disposition in skeletal muscle was studied in the isolated perfused rat hindquarter. 2. Insulin and exercise, induced by sciatic-nerve stimulation, enhanced glucose uptake about tenfold in fed and starved rats, but were without effect in rats with diabetic ketoacidosis. 3. At rest, the oxidation of lactate (0.44 mumol/min per 30 g muscle in fed rats) was decreased by 75% in both starved and diabetic rats, whereas the release of alanine and lactate (0.41 and 1.35 mumol/min per 30 g respectively in the fed state) was increased. Glycolysis, defined as the sum of lactate+alanine release and lactate oxidation, was not decreased in either starvation or diabetes. 4. In all groups, exercise tripled O2 consumption (from approximately 8 to approximately 25 mumol/min per 30 g of muscle) and increased the release and oxidation of lactate five- to ten-fold. The differences in lactate release between fed, starved and diabetic rats observed at rest were no longer apparent; however, lactate oxidation was still several times greater in the fed group. 5. Perfusion of the hindquarter of a fed rat with palmitate, octanoate or acetoacetate did not alter glucose uptake or lactate release in either resting or exercising muslce; however, lactate oxidation was significantly inhibited by acetoacetate, which also increased the intracellular concentration of acetyl-CoA. 6. The data suggest that neither that neither glycolysis nor the capacity for glucose transport are inhbitied in the perfused hindquarter during starvation or perfusion with fatty acids or ketone bodies. On the other hand, lactate oxidation is inhibited, suggesting diminished activity of pyruvate dehydrogenase. 7. Differences in the regulation of glucose metabolism in heart and skeletal muscle and the role of the glucose/fatty acid cycle in each tissue are discussed.

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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