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.

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.

scholarly journals Histidine Promotes the Glucose Synthesis through Activation of the Gluconeogenic Pathway in Bovine Hepatocytes

Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3295
Author(s):  
Tianyu Yang ◽  
Zhiqiang Cheng ◽  
Maocheng Jiang ◽  
Xiaoyu Ma ◽  
Osmond Datsomor ◽  
...  
Keyword(s):  
Mrna Level ◽  
Regulatory Effect ◽  
Hepatic Glucose Output ◽  
Grass Silage ◽  
Lactating Cows ◽  
Hepatic Glucose ◽  
Glucose Synthesis ◽  
Limiting Amino Acid ◽  
Glucose Output

Histidine (His) is considered to be the first-limiting amino acid (AA) on grass silage-based diets in lactation cows, which correlate positively with lactose yield. The higher glucose requirements of lactating cows can be met through a combination of increased capacity for gluconeogenesis and increased supply of gluconeogenic precursors. However, the effect of His on the expression of gluconeogenic genes in the bovine hepatocytes is less known. Therefore, this study aimed to investigate the regulatory effect of His on the key gluconeogenic genes and glucose output in bovine hepatocytes. The addition of 0.15, 0.6, and 1.2 mM His in a medium significantly enhanced (p < 0.05) the viability of bovine hepatocytes. Remarkably, 1.2 mM His induced profound changes (p < 0.05) in the mRNA level of key genes involved in gluconeogenesis, including PCK1, PCK2, FBP1, and G6PC in vitro. Furthermore, the mRNA expression of PCK1 was significantly elevated (p < 0.05) by the addition of 1.2 mM His at 3, 6, 12, and 24 h of incubation. The hepatic glucose output increased (p < 0.05) linearly with increasing His concentration. These findings indicate that the addition of His may be efficiently converted into glucose via the upregulation of genes related to the gluconeogenic pathway.

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.

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.

Effects of epinephrine on the net hepatic uptake of lactate, pyruvate, and glycerol in sheep

1991 ◽  
Vol 69 (4) ◽  
pp. 475-479 ◽  
Author(s):  
Ronald P. Brockman
Keyword(s):  
Blood Vessels ◽  
Glucose Production ◽  
Hepatic Uptake ◽  
Metabolic Clearance ◽  
Hepatic Extraction ◽  
Hepatic Glucose Output ◽  
Epinephrine Infusion ◽  
Hepatic Gluconeogenesis ◽  
Hepatic Glucose ◽  
Glucose Output

Epinephrine causes hyperglycemia in part by increasing gluconeogenesis. However, the mechanism of its gluconeogenic effects has not been studied in ruminants. This study was undertaken to examine the effect of epinephrine on the net hepatic uptake of selected glucose precursors in sheep. The major abdominal blood vessels of the sheep were catheterized in normal and alloxan diabetic sheep. Glucose production, metabolic clearance of glucose, and the hepatic removal of certain glucose precursors were determined before, during, and after epinephrine infusion. Epinephrine increased the hepatic glucose output, the concentrations of lactate and glycerol in plasma, and the net hepatic uptake and fractional hepatic extraction of lactate and glycerol. These effects were independent of changes in the concentrations of insulin and glucagon in plasma. These results show that epinephrine directly stimulates hepatic gluconeogenesis in sheep.Key words: epinephrine, hepatic gluconeogenesis, sheep.

Evidence for dual control mechanism regulating hepatic glucose output in nondiabetic men

Diabetes ◽  
1991 ◽  
Vol 40 (8) ◽  
pp. 1033-1040 ◽  
Author(s):  
J. N. Clore ◽  
P. S. Glickman ◽  
S. T. Helm ◽  
J. E. Nestler ◽  
W. G. Blackard
Keyword(s):  
Control Mechanism ◽  
Dual Control ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output
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