Quantitation of Hepatic Glycogenolysis And Gluconeogenesis in Fasting Humans With
            <sup>13</sup>
            C NMR

Rothman, Douglas L.; Magnusson, Inger; Katz, Lee D.; Shulman, Robert G.; Shulman, Gerald I.

doi:10.1126/science.1948033

Cited by 485 publications

(427 citation statements)

References 27 publications

Supporting

Mentioning

399

Contrasting

Unclassified

Order By: Relevance

“…This value is very close to the basal glucose production observed in healthy subjects after an overnight fast (Gerich, 1993), and may at ®rst sight suggest that endogenous glucose production was not suppressed by either diet. This interpretation however would be erroneous (Rothman et al, 1991;Schneiter et al, 1999); a continuing systemic release of unlabeled glucose during 13 C carbohydrate absorption therefore re¯ects a continuing hepatic glycogenolysis at the same time as exogenous 13 C-labeled glucose is converted into liver glycogen. 13 C glucose appearance allowed us to estimate that approximately 64% of ingested carbohydrate appeared in the systemic circulation, suggesting that the other 36% were extracted by the splanchnic organs and converted into glycogen, at the same time as unlabeled glycogen was released.…”

Section: Resultsmentioning

confidence: 99%

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

et al. 2001

View full text Add to dashboard Cite

Objective: To assess whether b-glucan (which is fermented in the colon) lowers postprandial glucose concentrations through mechanisms distinct from a delayed carbohydrate absorption and inhibits de novo lipogenesis. Design: Administration of frequent small meals each hour over 9 h allows a rate of intestinal absorption to be reached which is independent of a delayed absorption. A group of 10 healthy men received either an isoenergetic diet containing 8.9 gaday b-glucan or without b-glucan for 3 days. On the third day, the diet was administered as fractioned meals ingested every hour for 9 h. Setting: Laboratory for human metabolic investigations. Subjects: Ten healthy male volunteers. Main outcome measures: Plasma glucose and insulin concentrations, glucose kinetics, glucose oxidation, de novo lipogenesis. Results: On the third day, plasma glucose and free fatty acid concentrations, carbohydrate and lipid oxidation, and energy expenditure were identical with b-glucan and cellulose. Plasma insulin concentrations were, however, 26% lower with b-glucan during the last 2 h of the 9 h meal ingestion. Glucose rate of appearance at steady state was 12% lower with b-glucan. This corresponded to a 21% reduction in the systemic appearance rate of exogenous carbohydrate with b-glucan, while endogenous glucose production was similar with both diets. De novo lipogenesis was similar with and without b-glucan. Conclusion: Administration of frequent meals with or without b-glucan results in similar carbohydrate and lipid metabolism. This suggests that the lowered postprandial glucose concentrations which are observed after ingestion of a single meal containing b-glucan are essentially due to a delayed and somewhat reduced carbohydrate absorption from the gut and do not result from the effects of fermentation products in the colon. Descriptors: glucose production; de novo lipogenesis; substrate oxidation

show abstract

Section: Resultsmentioning

confidence: 99%

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

et al. 2001

View full text Add to dashboard Cite

show abstract

“…VO 2 max 29 which is equivalent to the level of hepatic glycogen depletion following a 24-h fast. 30 Thus, exercise induces quantitatively larger muscle and hepatic substrate deficits than energy intake restriction. Such substrate deficits in muscle and/or liver may mediate the TG-lowering effects of exercise by stimulating skeletal muscle LPL activity and increasing TG clearance 31 and/or by directing the hepatic fatty acid flux towards oxidation and away from reesterification, thereby reducing VLDL production, 31,32 Thus greater energy substrate deficits in muscle tissue and liver could mediate the larger effect of exercise-induced, compared to dietary-induced deficits on TG metabolism.…”

Section: Discussionmentioning

confidence: 99%

Energy replacement attenuates the effects of prior moderate exercise on postprandial metabolism in overweight/obese men

et al. 2007

View full text Add to dashboard Cite

Background:The extent to which exercise-induced changes to postprandial metabolism are dependant on the associated energy deficit is not known. Objective: To determine the effects of exercise, with and without energy replacement, on postprandial metabolism. Design: Each subject underwent three 2-day trials in random order. On day 1 of each trial subjects rested (control), walked at 50% maximal oxygen uptake to induce a net energy expenditure of 27 kJ kg À1 body mass (energy-deficit) or completed the same walk with the net energy expended replaced (energy-replacement). On day 2 subjects completed an 8.5-h metabolic assessment. For 3 days prior to day 2, subjects consumed an isocaloric diet, avoided planned exercise (apart from exercise interventions) and alcohol. Subjects: A total of 13 overweight/obese men (age: 40 ± 8 years, body mass index: 31.1 ± 3.0 kg m À2 ). Measurements: Postprandial triglyceride, insulin, glucose, non-esterified fatty acid and 3-hydroxybutyrate concentrations and substrate utilization rates were determined. Results: Energy-deficit lowered postprandial triglyceride concentrations by 14 and 10% compared with control and energyreplacement (Po0.05 for both). Energy-deficit increased postprandial 3-hydroxybutyrate concentrations by 40 and 19% compared with control and energy-replacement (Po0.05 for both). Postprandial insulin concentrations were 18 and 10% lower for energy-deficit and energy-replacement compared with control and 10% lower for energy-deficit than energy-replacement (Po0.05 for all). Postprandial fat oxidation increased by 30 and 14% for energy-deficit and energy-replacement compared to control and was 12% higher for energy-deficit than energy-replacement (Po0.05 for all). Conclusion: Exercise with energy replacement lowered postprandial insulinaemia and increased fat oxidation. However an exercise-induced energy deficit augmented these effects and was necessary to lower postprandial lipaemia.

show abstract

“…If the measured concentrations are set to a straight line the rate must be constant. However, what is sought is an overall rate; Shulman and co-workers (Rothman et al 1991) did analyse segments with time. By the 2 H 2 O method the contribution of GNG increases and hence the contribution of glycogenolysis decreases.…”

Section: Nmr Spectroscopymentioning

confidence: 99%

Quantifying the contribution of gluconeogenesis to glucose production in fasted human subjects using stable isotopes

Landau

1999

Proc. Nutr. Soc.

View full text Add to dashboard Cite

The contribution of gluconeogenesis to glucose production is estimated from the enrichment of the H bound to C-5 of glucose relative to either that bound to C-2 of glucose or the enrichment in body water on ingesting 2H2O in the fasted state. Contributions of all gluconeogenic substrates are included in the estimate and the limitation of an uncertain precursor enrichment removed. The half-life of 2H2O in body water precludes a repeat study for many weeks. Glycogen cycling could result in underestimation, but there is evidence that glycogen cycling does not occur in liver in the fasted state. Gluconeogenesis has been estimated by mass-isotopomer-distribution analyses, usually by administering 13C-labelled glycerol. Underestimates emphasize the major limitation of the method, i.e. the need to assume a single enrichment of the precursor pool. Estimates of gluconeogenesis from isotopomer distribution in arterial-blood glucose and lactate on infusing [U-13C6] glucose are unreliable, as a proportion of the glucose is formed from glycerol and from amino acids not converted to glucose via pyruvate. Loss of label in the Krebs cycle and relying on enrichment of arterial-blood lactate as a measure of hepatic pyruvate further add to the uncertainty. Estimates of the rate of gluconeogenesis by NMR are obtained by subtraction of the rate of glycogenolysis determined by NMR from the rate of glucose production. Estimates are then the mean rate for the period over which glycogen contents are measured. Technical considerations can limit the accuracy of analyses and result in overestimates.

show abstract

Quantitation of Hepatic Glycogenolysis And Gluconeogenesis in Fasting Humans With ¹³ C NMR

Cited by 485 publications

References 27 publications

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

Energy replacement attenuates the effects of prior moderate exercise on postprandial metabolism in overweight/obese men

Quantifying the contribution of gluconeogenesis to glucose production in fasted human subjects using stable isotopes

Contact Info

Product

Resources

About

Quantitation of Hepatic Glycogenolysis And Gluconeogenesis in Fasting Humans With 13 C NMR

Cited by 485 publications

References 27 publications

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

Mechanisms of action of β-glucan in postprandial glucose metabolism in healthy men

Energy replacement attenuates the effects of prior moderate exercise on postprandial metabolism in overweight/obese men

Quantifying the contribution of gluconeogenesis to glucose production in fasted human subjects using stable isotopes

Contact Info

Product

Resources

About

Quantitation of Hepatic Glycogenolysis And Gluconeogenesis in Fasting Humans With ¹³ C NMR