The effect of xylazine upon hepatic glucose production and blood flow rate in the lactating dairy cow

1976 ◽  
Vol 99 (12) ◽  
pp. 234-236 ◽  
Author(s):  
H. Symonds
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Dairy Cow ◽  
Hepatic Glucose Production ◽  
Blood Flow Rate ◽  
Glucose Production ◽  
Hepatic Glucose

Glucose production during exercise in humans: a-hv balance and isotopic-tracer measurements compared

1999 ◽  
Vol 87 (1) ◽  
pp. 111-115 ◽  
Author(s):  
R. Bergeron ◽  
M. Kjaer ◽  
L. Simonsen ◽  
J. Bülow ◽  
H. Galbo
Keyword(s):  
Blood Flow ◽  
Continuous Infusion ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Dilution Method ◽  
Hepatic Glucose ◽  
Balance Technique ◽  
Tracer Dilution ◽  
Exercise In Humans

The present study compared the arteriohepatic venous (a-hv) balance technique and the tracer-dilution method for estimation of hepatic glucose production during both moderate and heavy exercise in humans. Eight healthy young men (aged 25 yr; range, 23–30 yr) performed semisupine cycling for 40 min at 50.4 ± 1.5(SE)% maximal O2 consumption, followed by 30 min at 69.0 ± 2.2% maximal O2 consumption. The splanchnic blood flow was estimated by continuous infusion of indocyanine green, and net splanchnic glucose output was calculated as the product of splanchnic blood flow and a-hv blood glucose concentration differences. Glucose appearance rate was determined by a primed, continuous infusion of [3-3H]glucose and was calculated by using formulas for a modified single compartment in non-steady state. Glucose production was similar whether determined by the a-hv balance technique or by the tracer-dilution method, both at rest and during moderate and intense exercise ( P > 0.05). It is concluded that, during exercise in humans, determination of hepatic glucose production can be performed equally well with the two techniques.

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.

Effects of a Dobutamine-induced Increase in Splanchnic Blood Flow on Hepatic Metabolic Activity in Patients with Septic Shock 

1997 ◽  
Vol 86 (4) ◽  
pp. 818-824 ◽  
Author(s):  
Helmut Reinelt ◽  
Peter Radermacher ◽  
Gunther Fischer ◽  
Wolfgang Geisser ◽  
Ulrich Wachter ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Volume Resuscitation ◽  
Hepatic Glucose ◽  
Splanchnic Oxygen

Background Septic shock leads to increased splanchnic blood flow (Qspl) and oxygen consumption (VO2spl). The increased Qspl, however may not match the splanchnic oxygen demand, resulting in hepatic dysfunction. This concept of ongoing tissue hypoxia that can be relieved by increasing splanchnic oxygen delivery (DO2spl), however, was challenged because most of the elevated VO2spl was attributed to increased hepatic glucose production (HGP) resulting from increased substrate delivery. Therefore the authors tested the hypothesis that a dobutamine-induced increase in Qspl and DO2spl leads to increased VO2spl associated with accelerated HGP in patients with septic shock. Methods Twelve patients with hyperdynamic septic shock in whom blood pressure had been stabilized (mean arterial pressure > or = 70 mmHg) with volume resuscitation and norepinephrine received dobutamine to obtain a 20% increase in cardiac index (CI). Qspl, DO2spl, and VO2spl were assessed using the steady-state indocyanine green clearance technique with correction for hepatic dye extraction, and HGP was determined from the plasma appearance rate of stable, non-radio-active-labeled glucose using a primed-constant infusion approach. Results Although the increase in CI resulted in a similar increase in Qspl (from 0.91 +/- 0.21 to 1.21 +/- 0.34l.min-1.m2; P < 0.001) producing a parallel increase of DO2spl (from 141 +/- 33 to 182 +/- 44 ml.min-1.m2; P < 0.001), there was no effect on VO2spl (73 +/- 16 and 82 +/- 21 ml.min-1.m2, respectively). Hepatic glucose production decreased from 5.1 +/- 1.6 to 3.6 +/- 0.9 mg.kg-1.min-1 (P < 0.001). Conclusions In the patients with septic shock in whom blood pressure had been stabilized with volume resuscitation and norepinephrine, no delivery-dependency of VO2spl could be detected. Oxygen consumption was not related to the accelerated HGP either, and thus the concept that HGP dominates VO2spl must be questioned in well-resuscitated patients with septic shock.

Relationship between arterial and portal vein immunoreactive glucagon during exercise

1993 ◽  
Vol 75 (2) ◽  
pp. 724-729 ◽  
Author(s):  
D. H. Wasserman ◽  
D. B. Lacy ◽  
D. P. Bracy
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Portal Vein ◽  
Indocyanine Green ◽  
Treadmill Exercise ◽  
Hepatic Glucose Production ◽  
Liver Blood Flow ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Flow Through

The importance of changes in glucagon in the regulation of hepatic glucose production (Ra) during exercise has been questioned, as an increase in arterial immunoreactive glucagon (IRG) is not always detectable. However, IRG in the portal vein (PV) and not in the artery is most relevant, as flow through PV is approximately 80% of liver blood flow. To assess the extent that arterial IRG reflects the levels the liver is exposed to in PV, dogs (n = 5) were implanted with catheters in a carotid artery, hepatic vein (HV), and PV. Dogs were studied > or = 16 days later during rest and 150 min of moderate treadmill exercise, with indocyanine green and [3–3H]glucose infused to assess hepatic plasma flow (HPF) and hepatic Ra. IRG was 66 +/- 7, 73 +/- 8, and 81 +/- 7 pg/ml in the artery, HV, and PV at rest; it rose at 10 and 150 min of exercise to 89 +/- 9 and 127 +/- 13 pg/ml in the artery, 106 +/- 17 and 186 +/- 21 pg/ml in HV, and, by considerably more, to 153 +/- 20 and 261 +/- 25 pg/ml in PV. HPF fell by approximately 30% with exercise. The fall in HPF accounted for < 11% of the increased arterial-to-PV IRG gradient during exercise, with increased splanchnic IRG release comprising the remainder. Ra was linearly related to IRG levels in the three vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

FoxO3 regulates hepatic glucose production

2013 ◽  
Vol 51 (01) ◽  
Author(s):  
S Gul ◽  
KH Holzmann ◽  
F Leithäuser ◽  
H Maier ◽  
B Böhm ◽  
...  
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

Hyperglycemia per se does not inhibit hepatic glucose production in man

1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S20
Author(s):  
M.J. MÜLLER ◽  
K.J. ACHESON ◽  
A. G. BURGER ◽  
E. JEQUIER ◽  
A. VON ZUR MÜHLEN
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Per Se

Regulation of Hepatic Glucose Production by Transforming Growth Factor Beta 1 via Protein Kinase A

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2441-PUB ◽  
Author(s):  
QUAN PAN ◽  
YUNMEI CHEN ◽  
HUI YAN ◽  
WANBAO YANG ◽  
ZHENG SHEN ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Growth Factor Beta ◽  
Kinase A

64-LB: Aerobic Exercise Decreases Hepatic Glucose Production via Asprosin Pathway in Diabetic Rats

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 64-LB
Author(s):  
JEONGRIM KO ◽  
TAE NYUN KIM ◽  
DAE YUN SEO ◽  
JIN HAN
Keyword(s):  
Aerobic Exercise ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose

The role of autoregulation of the hepatic glucose production in man. Response to a physiologic decrement in plasma glucose

Diabetes ◽  
1986 ◽  
Vol 35 (2) ◽  
pp. 186-191 ◽  
Author(s):  
I. Hansen ◽  
R. Firth ◽  
M. Haymond ◽  
P. Cryer ◽  
R. Rizza
Keyword(s):  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose
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