scholarly journals Acetaminophen glucuronide and plasma glucose report identical estimates of gluconeogenesis and glycogenolysis for healthy and prediabetic subjects using the deuterated water method

2012 ◽  
Vol 70 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Cristina Barosa ◽  
John G. Jones ◽  
Robert Rizza ◽  
Ananda Basu ◽  
Rita Basu
Keyword(s):  
Plasma Glucose ◽  
Deuterated Water ◽  
Acetaminophen Glucuronide

scholarly journals Resolving the Sources of Plasma Glucose Excursions following a Glucose Tolerance Test in the Rat with Deuterated Water and [U-13C]Glucose

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e34042 ◽  
Author(s):  
Teresa C. Delgado ◽  
Cristina Barosa ◽  
Patrícia M. Nunes ◽  
Sebastián Cerdán ◽  
Carlos F. G. C. Geraldes ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Deuterated Water

Simplified analysis of acetaminophen glucuronide for quantifying gluconeogenesis and glycogenolysis using deuterated water

2015 ◽  
Vol 479 ◽  
pp. 37-39 ◽  
Author(s):  
J. Jones ◽  
S. Kahl ◽  
F. Carvalho ◽  
C. Barosa ◽  
M. Roden
Keyword(s):  
Deuterated Water ◽  
Simplified Analysis ◽  
Acetaminophen Glucuronide

Measurement of gluconeogenesis by deuterated water: the effect of equilibration time and fasting period

2006 ◽  
Vol 290 (6) ◽  
pp. E1212-E1217 ◽  
Author(s):  
Gideon Allick ◽  
Saskia N. van der Crabben ◽  
Mariette T. Ackermans ◽  
Erik Endert ◽  
Hans P. Sauerwein
Keyword(s):  
Plasma Glucose ◽  
Healthy Subjects ◽  
Hepatic Glycogen ◽  
Equilibration Time ◽  
Deuterated Water ◽  
Healthy Male ◽  
Reliable Measurement ◽  
Fasting Period ◽  
Incubation Periods ◽  
Male Subjects

Fasting gluconeogenesis (GNG) is often quantified using the 2H2O technique, which is based on plasma 2H2O enrichment and ensuing enrichment of plasma glucose at the C5 and C2 positions. Fractional (fr)GNG can be calculated using the ratio of C5 to C2 enrichment or the ratio of C5 to plasma 2H2O enrichment. For the latter, equilibration of 2H2O and C2 is required. The optimal equilibration period of 2H2O and C2 remains to be elucidated. In six healthy male subjects fasted for 18 h, we studied the effects of 3-, 5-, and 15-h 2H2O incubation periods on 1) the equilibration of plasma 2H2O and C2 glucose enrichment, 2) the measurement of frGNG, and 3) C5 labeling of hepatic glycogen after 1 mg of glucagon administration. After 3-h 2H2O incubation, plasma 2H2O and C2 were not equilibrated, frGNG C5/2H2O and C5/C2 were also different as was gluconeogenesis calculated with C5/2H2O and C5/C2. After 5- and 15-h 2H2O incubation, plasma 2H2O and C2 were equilibrated, and frGNG C5/2H2O and C5/C2 were similar, as was GNG calculated with C5/2H2O and C5/C2. After glucagon administration, no difference of C5 enrichment was found between 3, 5, and 15 h of 2H2O incubation. In conclusion, for reliable measurement of GNG in healthy subjects with C5/2H2O incubation periods longer than 3 h are required. After 5- and 15-h 2H2O incubation, GNG can be reliably measured with C5/2H2O. Gluconeogenetic labeling of glycogen did not affect the results after 3, 5, or 15 h of 2H2O incubation.

2H enrichment distribution of hepatic glycogen from 2H2O reveals the contribution of dietary fructose to glycogen synthesis

2013 ◽  
Vol 304 (4) ◽  
pp. E384-E391 ◽  
Author(s):  
Teresa C. Delgado ◽  
Fátima O. Martins ◽  
Filipa Carvalho ◽  
Ana Gonçalves ◽  
Donald K. Scott ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glycogen Synthesis ◽  
Krebs Cycle ◽  
Hepatic Glycogen ◽  
Deuterated Water ◽  
Indirect Pathway ◽  
Triose Phosphate ◽  
Glucose Levels ◽  
Dietary Fructose ◽  
Glucose Synthesis

Dietary fructose can benefit or hinder glycemic control, depending on the quantity consumed, and these contrasting effects are reflected by alterations in postprandial hepatic glycogen synthesis. Recently, we showed that 2H enrichment of glycogen positions 5 and 2 from deuterated water (2H2O) informs direct and indirect pathway contributions to glycogenesis in naturally feeding rats. Inclusion of position 6 S 2H enrichment data allows indirect pathway sources to be further resolved into triose phosphate and Krebs cycle precursors. This analysis was applied to six rats that had fed on standard chow (SC) and six rats that had fed on SC plus 35% sucrose in their drinking water (HS). After 2 wk, hepatic glycogenesis sources during overnight feeding were determined by 2H2O administration and postmortem analysis of glycogen 2H enrichment at the conclusion of the dark period. Net overnight hepatic glycogenesis was similar between SC and HS rodents. Whereas direct pathway contributions were similar (403 ± 71 μmol/g dry wt HS vs. 578 ± 76 μmol/g dry wt SC), triose phosphate contributions were significantly higher for HS compared with SC (382 ± 61 vs. 87 ± 24 μmol/g dry wt, P < 0.01) and Krebs cycle inputs lower for HS compared with SC (110 ± 9 vs. 197 ± 32 μmol/g dry wt, P < 0.05). Analysis of plasma glucose 2H enrichments at the end of the feeding period also revealed a significantly higher fractional contribution of triose phosphate to plasma glucose levels in HS vs. SC. Hence, the 2H enrichment distributions of hepatic glycogen and glucose from 2H2O inform the contribution of dietary fructose to hepatic glycogen and glucose synthesis.

Acetaminophen glucuronidation accurately reflects gluconeogenesis in fasted dogs

1996 ◽  
Vol 271 (3) ◽  
pp. E529-E534 ◽  
Author(s):  
W. F. Schwenk ◽  
J. C. Kahl
Keyword(s):  
Plasma Glucose ◽  
Specific Activity ◽  
Glucose Flux ◽  
Diphosphate Glucose ◽  
The Mean ◽  
Acetaminophen Glucuronide ◽  
To Come

To assess whether acetaminophen glucuronide accurately reflects uridyl diphosphate-glucose (UDP-glucose) derived from gluconeogenesis during fasting, three mongrel dogs received infusions of [U-14C]lactate, [1-13C]galactose, and [6-3H]glucose (after fasting overnight or for 2.5 days). After initiation of the isotopes (3 h), acetaminophen was given, and the urinary acetaminophen glucuronide was isolated. The mean plasma [14C]glucose specific activity (SA) was similar to the mean urinary acetaminophen glucuronide SA both after fasting overnight [299 +/- 19 vs. 296 +/- 14 disintegrations.min-1 (dpm).mumol-1, respectively] and after 2.5 days of fasting (511 +/- 8 vs. 562 +/- 32 dpm/mumol, respectively). Mean plasma glucose flux calculated using [6-3H]glucose decreased (P < 0.05) with two additional days of fasting (18.7 +/- 1.2 vs. 13.6 +/- 0.6 mumol.kg-1.min-1), as did intrahepatic (P < 0.05) UDP-glucose flux measured using [1-13C]galactose (8.6 +/- 0.7 vs. 5.5 +/- 0.3 mumol.kg-1.min-1). We conclude that, in fasted dogs, plasma glucose and UDP-glucose, as sampled by acetaminophen, equally reflect gluconeogenesis and appear to come from the same pool of glucose 6-phosphate. In addition, cycling of glucose moieties through UDP-glucose and glycogen decreases with an increased period of fasting.

Fasting Plasma Glucose Test Called Inadequate

2005 ◽  
Vol 39 (4) ◽  
pp. 1-3
Author(s):  
KATE JOHNSON
Keyword(s):  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Fasting Plasma ◽  
Glucose Test

Childhood Plasma Glucose May Predict Adult Diabetes

2010 ◽  
Vol 40 (3) ◽  
pp. 16
Author(s):  
MARY ANN MOON
Keyword(s):  
Plasma Glucose ◽  
Adult Diabetes

No Evidence for Short-Term Regulation of Plasminogen Activator Inhibitor Activity by Insulin in Man

1992 ◽  
Vol 67 (01) ◽  
pp. 117-120 ◽  
Author(s):  
Helena Vuorinen-Markkola ◽  
llpo Puhakainen ◽  
Hannele Yki-Järvinen
Keyword(s):  
Plasminogen Activator ◽  
Plasma Glucose ◽  
Serum Triglyceride ◽  
Plasminogen Activator Inhibitor ◽  
Saline Infusion ◽  
Serum Triglycerides ◽  
Serum Free ◽  
Free Insulin ◽  
Activator Inhibitor ◽  
Pai 1

SummaryIn crossectional studies a positive correlation has been found between circulating insulin, triglycerides and plasminogen activator inhibitor (PAI-1) activity. To directly examine the effect of insulin on PAI-1 activity in vivo, we determined the response of PAI-1 activity in 17 normal subjects to acute hyperinsulinemia (serum free insulin 92 ± 8 mU/l) during maintenance of normoglycemia (plasma glucose 5.1 ± 0.1 mmol/l). In 12 matched control subjects PAI-1 activity was measured during infusion of saline (serum free insulin 3.6 ± 0.3 mU/l, plasma glucose 5.2 ± 0.1 mmol/l). Plasma PAI-1 activity decreased during the insulin infusion from 9.0 α 1.4 to 5.6 α 0.8 U/ml (p <0.01), and during saline infusion from 7.0 ± 1.4 to 4.3 ± 0.6 U/ml (p <0.05). Serum triglyceride concentrations decreased from 1.09 ± 0.20 to 0.76 ± 0.09 mmol/l (p < 0.001) during hyperinsulinemia but remained unchanged during the saline infusion (1.04 ± 0.11 vs. 1.02 ± 0.12 mmol/l, NS). We conclude that insulin does not acutely change plasma PAI-1 activity, and that acute insulin-induced changes in serum triglycerides occur independently from those of PAI-1 activity.

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