Hepatic lactate uptake versus leg lactate output during exercise in humans

2007 ◽  
Vol 103 (4) ◽  
pp. 1227-1233 ◽  
Author(s):  
H. B. Nielsen ◽  
M. A. Febbraio ◽  
P. Ott ◽  
P. Krustrup ◽  
N. H. Secher
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Prolonged Exercise ◽  
Incremental Exercise ◽  
Hepatic Glucose Output ◽  
Arterial Lactate ◽  
Hepatic Glucose ◽  
Lactate Output ◽  
Lactate Uptake ◽  
Glucose Output

The exponential rise in blood lactate with exercise intensity may be influenced by hepatic lactate uptake. We compared muscle-derived lactate to the hepatic elimination during 2 h prolonged cycling (62 ± 4% of maximal O2 uptake, V̇o2max) followed by incremental exercise in seven healthy men. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermodilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 ± 0.5 vs. 6.5 ± 0.6 mmol/min; mean ± SE) and at an arterial lactate of 2.0 ± 0.2 mM, the leg lactate output of 3.0 ± 1.8 mmol/min was about fourfold higher than the hepatic lactate uptake (0.7 ± 0.3 mmol/min). During incremental exercise, the hepatic glucose output was about one-third of the leg glucose uptake (2.0 ± 0.4 vs. 6.2 ± 1.3 mmol/min) and the arterial lactate reached 6.0 ± 1.1 mM because the leg lactate output of 8.9 ± 2.7 mmol/min was markedly higher than the lactate taken up by the liver (1.1 ± 0.6 mmol/min). Compared with prolonged exercise, the hepatic lactate uptake increased during incremental exercise, but the relative hepatic lactate uptake decreased to about one-tenth of the lactate released by the legs. This drop in relative hepatic lactate extraction may contribute to the increase in arterial lactate during intense exercise.

Dynamics of hepatic lactate and glucose balances during prolonged exercise and recovery in the dog

1987 ◽  
Vol 63 (6) ◽  
pp. 2411-2417 ◽  
Author(s):  
D. H. Wasserman ◽  
D. B. Lacy ◽  
D. R. Green ◽  
P. E. Williams ◽  
A. D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Production ◽  
Moderate Intensity ◽  
Hepatic Veins ◽  
Hepatic Glucose Output ◽  
Rapid Release ◽  
Hepatic Glucose ◽  
Lactate Output ◽  
Glucose Output ◽  
Hepatic Glucose Uptake

The present experiments were undertaken to assess dynamics of hepatic lactate and glucose balance in the over-night-fasted dog during 150 min of moderate-intensity treadmill exercise and 90 min of exercise recovery. Catheters were implanted chronically in an artery and portal and hepatic veins 16 days before experimentation. 3–3H-glucose was infused to determine hepatic glucose uptake, as well as tracer-determined glucose production by isotope dilution (Ra). At rest, net hepatic lactate output was 0.33 +/- 0.15 mg.kg-1.min-1 and increased to 2.26 +/- 0.82 mg.kg-1.min-1 after 10 min of exercise, after which it fell such that the liver was a net lactate consumer by the end of exercise and through recovery. In contrast to the rapid release of lactate, net hepatic glucose output rose gradually from 2.58 +/- 0.20 mg.kg-1.min-1 at rest to 8.87 +/- 0.85 mg.kg-1.min-1 after 60 min of exercise, beyond which it did not change significantly until the cessation of exercise. Hepatic glucose uptake at rest was 1.38 +/- 0.42 mg.kg-1.min-1 and did not change appreciably during exercise or recovery. Absolute hepatic glucose output (net glucose output plus uptake) rose from 3.96 +/- 0.45 mg.kg-1.min-1 at rest to 10.20 +/- 1.09 mg.kg-1.min-1 after 60 min of exercise and was 9.65 +/- 1.15 mg.kg-1.min-1 at 150 min of exercise. Ra rose from 3.34 +/- 0.21 mg.kg-1.min-1 to 7.58 +/- 0.73 and 8.59 +/- 0.77 mg.kg-1.min-1 at 60 and 150 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin as a mediator of hepatic glucose uptake in the conscious dog

1982 ◽  
Vol 242 (2) ◽  
pp. E97-E101 ◽  
Author(s):  
A. D. Cherrington ◽  
P. E. Williams ◽  
N. Abou-Mourad ◽  
W. W. Lacy ◽  
K. E. Steiner ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Plasma Insulin ◽  
Marked Effect ◽  
Glucose Infusion ◽  
Hepatic Glucose Output ◽  
Intravenous Glucose ◽  
Conscious Dog ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Hepatic Glucose Uptake

The aim of this study was to determine whether a physiological increment in plasma insulin could promote substantial hepatic glucose uptake in response to hyperglycemia brought about by intravenous glucose infusion in the conscious dog. To accomplish this, the plasma glucose level was doubled by glucose infusion into 36-h fasted dogs maintained on somatostatin, basal glucagon, and basal or elevated intraportal insulin infusions. In the group with basal glucagon levels and modest hyperinsulinemia (33 +/- 2 micro U/ml), the acute induction of hyperglycemia (mean increment of 120 mg/dl) caused marked net hepatic glucose uptake (3.7 +/- 0.5 mg . kg-1 . min-1). In contrast, similar hyperglycemia brought about in the presence of basal glucagon and basal insulin levels described net hepatic glucose output in 56%, but did not cause net hepatic glucose uptake. The length of fast was not crucial to the response because similar signals (insulin, 38 +/- 6 micro U/ml; glucose increment, 127 mg/dl) promoted identical net hepatic glucose uptake (3.8 +/- 0.6 mg . kg-1 . min-1) in dogs fasted for only 16 h. In conclusion, in the conscious dog, a) physiologic increments in plasma insulin have a marked effect on the ability of hyperglycemia to stimulate net hepatic glucose uptake, and b) it is not necessary to administer glucose orally to promote substantial net hepatic glucose uptake.

Pressor doses of angiotensin II increase insulin-mediated glucose uptake in normotensive men

1993 ◽  
Vol 265 (3) ◽  
pp. E362-E366 ◽  
Author(s):  
R. R. Townsend ◽  
D. J. DiPette
Keyword(s):  
Angiotensin Ii ◽  
Glucose Uptake ◽  
Whole Body ◽  
Glucose Disposal ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Cast Doubt ◽  
Normotensive Subjects ◽  
Glucose Output ◽  
Biochemical Action

The effect of pressor doses of angiotensin II infused intravenously on insulin-mediated glucose uptake was determined in normotensive men. A 3-h hyperinsulinemic euglycemic clamp was employed in 14 normotensive subjects to determine insulin-mediated glucose uptake with or without an infusion of angiotensin II (approximately 15 ng.kg-1.min-1), which increased blood pressure by 20/15 mmHg (systolic/diastolic). Addition of angiotensin II increased whole body glucose uptake by 15% (9.2 +/- 0.5 vs. 10.8 +/- 0.8 mg.kg-1 x min-1; P = 0.011), and glucose oxidation (determined by indirect calorimetry) by 25% (4.0 +/- 0.3 vs. 4.9 +/- 0.4 mg.kg-1 x min-1; P < 0.05) over insulin alone. There was no significant increase in hepatic glucose output during angiotensin II infusion (2.2 +/- 0.1 vs. 2.4 +/- 0.1 mg.kg-1 x min-1; P = NS). We conclude that angiotensin II in pressor doses increases insulin-mediated glucose disposal and oxidation. The mechanism for this may involve a redirection of blood flow into skeletal muscle during angiotensin II infusion or a direct biochemical action of angiotensin II. Although performed in lean normotensive subjects, these results cast doubt on a significant role for angiotensin II in the insulin resistance associated with essential hypertension.

scholarly journals Fetal Programming of Perivenous Glucose Uptake Reveals a Regulatory Mechanism Governing Hepatic Glucose Output During Refeeding

Diabetes ◽  
2003 ◽  
Vol 52 (6) ◽  
pp. 1326-1332 ◽  
Author(s):  
H. C. Murphy ◽  
G. Regan ◽  
I. G. Bogdarina ◽  
A. J.L. Clark ◽  
R. A. Iles ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Fetal Programming ◽  
Regulatory Mechanism ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output

scholarly journals Blood flow and nutrient exchange across the liver and gut of the dairy cow

1983 ◽  
Vol 49 (3) ◽  
pp. 481-496 ◽  
Author(s):  
M. A. Lomax ◽  
G. D. Baird
Keyword(s):  
Fatty Acids ◽  
Blood Flow ◽  
Flow Rate ◽  
Ketone Bodies ◽  
Blood Flow Rate ◽  
Hepatic Uptake ◽  
Hepatic Glucose Output ◽  
Lactating Cows ◽  
Hepatic Glucose ◽  
Glucose Output

1. The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting.2. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake.3. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptakes of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows.4. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine+threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting.5. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield.6. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

Measurement of hepatic glucose output and hepatic blood flow in response to glucagon

1959 ◽  
Vol 196 (2) ◽  
pp. 315-318 ◽  
Author(s):  
William C. Shoemaker ◽  
Theodore B. Van Itallie ◽  
William F. Walker
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Glucose Concentration ◽  
Base Line ◽  
Hepatic Glucose Output ◽  
Marked Rise ◽  
Hepatic Glucose ◽  
The Mean ◽  
Glucose Output ◽  
Venous Glucose

Arterial, portal and hepatic venous glucose concentrations and hepatic blood flow were simultaneously measured in nine dogs in the postabsorptive state, and after intravenous administration of glucagon. A marked rise in hepatic venous glucose concentration occurred promptly after glucagon administration. This rise coincided with a mean increase in estimated hepatic blood flow of approximately 100%. This increase in hepatic blood flow following the administration of glucagon was regularly observed in all animals; the increase in blood flow ranged from 41 to 204% in this series. Hepatic glucose output was calculated by multiplying the portal-hepatic vein gradient by the hepatic blood flow. The mean hepatic glucose output of the series increased from base line of 73 mg/min. to a maximum of 381 mg/min. in response to glucagon.

Plasma glucose and insulin responses to oral and intravenous glucose in cold-exposed humans

1988 ◽  
Vol 65 (6) ◽  
pp. 2395-2399 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Frim ◽  
M. F. Kavanagh
Keyword(s):  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Carbohydrate Metabolism ◽  
Cold Exposure ◽  
Plasma Glucose ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Oral Gtt ◽  
Glucose Output ◽  
Insulin Responses

Although glucose tolerance and skeletal muscle glucose uptake are markedly improved by cold exposure in animals, little is known about such responses in humans. This study used two variations of a glucose tolerance test (GTT) to investigate changes in carbohydrate metabolism in healthy males during nude exposure to cold. In experiment 1, an oral GTT was performed in the cold and in the warm (3 h at 10 or 29 degrees C). To bypass the gastrointestinal tract, and to suppress hepatic glucose output, a second experiment was carried out as described above, using an intravenous GTT. Even though cold exposure raised metabolic rate greater than 2.5 times, plasma glucose and insulin responses to an oral GTT remained unaltered. In contrast, cold exposure reduced the entire plasma glucose profile as a function of time during the intravenous GTT (P less than 0.05), as plasma glucose was returned to basal levels within 1 h in comparison to a full 2 h in the warm, despite low insulin levels. The results of the intravenous GTT demonstrate that even with low insulin levels, carbohydrate metabolism is increased in cold-exposed males. This effect could be masked in the oral GTT by gastrointestinal factors and a high hepatic glucose output. Cold exposure may enhance insulin sensitivity and/or responsiveness for glucose uptake, mainly in shivering skeletal muscles.

Mechanisms of postabsorptive hyperglycemia in streptozotocin diabetic rats

1996 ◽  
Vol 270 (5) ◽  
pp. E752-E758 ◽  
Author(s):  
J. K. Wi ◽  
J. K. Kim ◽  
J. H. Youn
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Diabetic Rats ◽  
Normal Rate ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Clearance ◽  
Streptozotocin Diabetic Rats ◽  
Acute Changes ◽  
Glucose Output

Postabsorptive hepatic glucose output (HGO) was estimated in normal (n = 9) and streptozotocin (STZ) diabetic rats after a 6-h [3-3H]glucose infusion. In diabetic rats, HGO was estimated at ambient (n = 12) or normal (achieved via phlorizin infusion; n = 9) glucose concentrations. HGO was not statistically different between normal and diabetic rats (63 +/- 3 vs. 77 +/- 10 mumol.kg-1.min-1; P> 0.05). HGO was also normal in diabetic rats even when plasma glucose was normalized with phlorizin infusion (71 +/- 5 vs. 63 +/- 3 mumol.kg-1.min-1; P> 0.05). In contrast, peripheral glucose uptake, when estimated at matched euglycemia, was lower by approximately 25% in diabetic than in normal rate (46 +/- 6 vs. 62 +/- 3 mumol.kg-1.min-1; P < 0.01). In addition, acute changes in plasma glucose concentrations did not have significant effects on HGO or peripheral glucose uptake in diabetic rats (P> 0.05), resulting in markedly decreased glucose clearance at ambient hyperglycemia (P < 0.001). In conclusion, postabsorptive HGO was not elevated in a majority (17 of 21) of STZ diabetic rats with severe hyperglycemia and therefore was not responsible for postabsorptive hyperglycemia. Our data suggest that an impairment in the ability of glucose to regulate peripheral glucose uptake or HGO develops in STZ diabetes and contributes to postabsorptive hyperglycemia.

Hepatic glucose production is more sensitive to insulin-mediated inhibition than hepatic VLDL-triglyceride production

2006 ◽  
Vol 291 (6) ◽  
pp. E1360-E1364 ◽  
Author(s):  
Marion A. M. den Boer ◽  
Peter J. Voshol ◽  
Folkert Kuipers ◽  
Johannes A. Romijn ◽  
Louis M. Havekes
Keyword(s):  
Glucose Uptake ◽  
Plasma Insulin ◽  
Hepatic Glucose Production ◽  
Plasma Concentrations ◽  
Hepatic Glucose Output ◽  
Insulin Levels ◽  
Hepatic Glucose ◽  
Plasma Insulin Levels ◽  
Glucose Output ◽  
Vldl Triglyceride

Insulin is an important inhibitor of both hepatic glucose output and hepatic VLDL-triglyceride (VLDL-TG) production. We investigated whether both processes are equally sensitive to insulin-mediated inhibition. To test this, we used euglycemic clamp studies with four increasing plasma concentrations of insulin in wild-type C57Bl/6 mice. By extrapolation, we estimated that half-maximal inhibition of hepatic glucose output and hepatic VLDL-TG production by insulin were obtained at plasma insulin levels of ∼3.6 and ∼6.8 ng/ml, respectively. In the same experiments, we measured that half-maximal decrease of plasma free fatty acid levels and half-maximal stimulation of peripheral glucose uptake were reached at plasma insulin levels of ∼3.0 and ∼6.0 ng/ml, respectively. We conclude that, compared with insulin sensitivity of hepatic glucose output, peripheral glucose uptake and hepatic VLDL-TG production are less sensitive to insulin.

Hepatic glycerol flux after E. coli endotoxin administration

1984 ◽  
Vol 247 (4) ◽  
pp. R687-R692 ◽  
Author(s):  
O. P. McGuinness ◽  
J. J. Spitzer
Keyword(s):  
Blood Flow ◽  
Clearance Rate ◽  
Arterial Blood Flow ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Metabolic Clearance Rate ◽  
Endotoxin Administration ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Glucose Output

Hepatic glycerol flux was examined in dogs after the administration of Escherichia coli endotoxin (0.4 mg/kg) to determine the contribution of the liver to the previously observed decline in the metabolic clearance rate of glycerol. Hepatic glycerol flux was estimated by determining hepatic arterial and portal venous blood flows with electromagnetic flow probes and by measuring arteriovenous difference of glycerol across the liver. Administration of endotoxin significantly decreased total hepatic blood flow (by approximately 20%) but did not alter hepatic arterial blood flow. Hepatic glycerol clearance decreased by 25–30% after endotoxin administration. Hepatic glycerol extraction also decreased. Under control conditions, 60% of the metabolic clearance rate of glycerol was attributable to the liver, whereas in the postendotoxin state approximately 72% of the glycerol clearance could be accounted for by hepatic clearance. Thus changes in transhepatic glycerol flux are only partially responsible for the previously observed alterations in glycerol clearance after endotoxin administration. Although hepatic glycerol clearance decreased, net hepatic glycerol, as well as lactate and alanine, uptake did not decrease, indicating that gluconeogenic precursor availability to the hepatocytes was not diminished. Hepatic glucose output was elevated after endotoxin administration. Changes in hepatic glucose output and gluconeogenic precursor uptake help explain the endotoxin-induced alternations in the fluxes of these metabolites.

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