Correction for metabolic exchange in the calculation of the rate of gluconeogenesis in rats

Hetenyi, G; Ferrarotto, C.

doi:10.1016/0006-2944(83)90073-x

Cited by 45 publications

(40 citation statements)

References 9 publications

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“…Using this line ofreasoning and the data in Table II it can be determined that the dilution factor at 90 min was 2.5±0.4 and at 180 min was 2.3±0.2 (P < NS). It is unclear why this estimate is so much larger than the 1.38 estimate of Hetenyi (10). Although Hetenyi's factor was calculated for [2-`4C] pyruvate, and our pyruvate was predominantly labeled in the C3 position, the factor for C3 pyruvate is in nearly all conditions less than that for C2 pyruvate (1 1).…”

Section: Discussionmentioning

confidence: 62%

Quantitative analysis of glycogen repletion by nuclear magnetic resonance spectroscopy in the conscious rat.

Shulman¹,

Rossetti²,

Rothman³

et al. 1987

J. Clin. Invest.

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In order to directly determine the amount of label exchange that occurs in the tricarboxylic cycle from labeled alanine and lactate after the ingestion of a glucose load 11-'3Cjglucose was administered by continuous intraduodenal infusion to awake catheterized rats to achieve steady state jugular venous glycemia (160 mg/dl) for 180 min. Liver was freeze-clamped at 90 and 180 min, and perchloric acid extracts of the liver were subjected to '3C and 'H nuclear magnetic resonance analysis. Dilution in the oxaloacetate pool was determined by comparing the intrahepatic 13C enrichments of C2, C3 positions of glutamate with the C2, C3 positions of alanine and lactate. In addition steady state flux equations were derived for calculation of relative fluxes through pyruvate dehydrogenase/TCA cycle flux and pyruvate kinase flux/total pyruvate utilization.After glucose ingestion in a 24-h fasted rat direct conversion ofglucose was responsible for 34% ofglycogen. The intrahepatic dilution factor for labeled pyruvate in the oxaloacetate pool was 2.4. Using this factor, alanine and lactate contributed -55% to glycogen formation. Pyruvate dehydrogenase flux ranged between 24 and 35% of total acetyl-coenzyme A (CoA) production and pyruvate kinase flux relative to total pyruvate utilization was 40%.

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Section: Discussionmentioning

confidence: 62%

Quantitative analysis of glycogen repletion by nuclear magnetic resonance spectroscopy in the conscious rat.

Shulman¹,

Rossetti²,

Rothman³

et al. 1987

J. Clin. Invest.

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“…Furthermore, recent data indicate that a substantial portion of the glycogen synthesized after glucose ingestion originates via the indirect pathway entailing gluconeogenesis from three-carbon precursors rather than from direct hepatic uptake of glucose (7,42 (44) have suggested a correction factor of approximately 2.2 for dilution of labeled by unlabeled precursors in the oxaloacetate pool during gluconeogenesis. Because this correction factor has only been validated in postabsorptive animals under steady-state conditions, its applicability to humans after meal ingestion remains uncertain.…”

Section: Resultsmentioning

confidence: 99%

Postprandial hyperglycemia in patients with noninsulin-dependent diabetes mellitus. Role of hepatic and extrahepatic tissues.

et al. 1986

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Patients with noninsulin-dependent diabetes mellitus (NIDDM) have both preprandial and postprandial hyperglycemia. To determine the mechanism responsible for the postprandial hyperglycemia insulin secretion, insulin action, and the pattern of carbohydrate metabolism after glucose ingestion were assessed in patients with NIDDM and in matched nondiabetic subjects using the dual isotope and forearm catheterization techniques. Prior to meal ingestion, hepatic glucose release was increased (P < 0.001) in the diabetic patients measured using [2-3Hj or 13-3HJ glucose. After meal ingestion, patients with NIDDM had excessive rates of systemic glucose entry (1,316±56 vs. 1,018±65 mg/kg 7 h, P < 0.01), primarily owing to a failure to suppress adequately endogenous glucose release (680±50 vs. 470±32 mg/kg-7 h, P < 0.01) from its high preprandial level. Despite impaired suppression of endogenous glucose production during a hyperinsulinemic glucose clamp (P < 0.001) and decreased postprandial C-peptide response (P <0.05) in NIDDM, percent suppression of hepatic glucose release after oral glucose was comparable in the diabetic and nondiabetic subjects (45±3 vs. 39±2%). Although new glucose formation from meal-derived three-carbon precursors (53±3 vs. 40±7 mg/kg 7 h, P < 0.05) was greater in the diabetic patients, it accounted for only a minor part of this excessive postprandial hepatic glucose release. Postprandial hyperglycemia was exacerbated by the lack of an appropriate increase in glucose uptake whether measured isotopically or by forearm glucose uptake. Thus as has been proposed for fasting hyperglycemia, excessive hepatic glucose release and impaired glucose uptake are involved in the pathogenesis of postprandial hyperglycemia in patients with NIDDM.

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“…Since this is neither corrected for dilution of label by carbon from the tricarboxylic acid cycle [20], nor accounts quantitatively for all substrates, it is considered an index of gluconeogenesis.…”

Section: Methodsmentioning

confidence: 99%

“…The value at 22 h of fasting in control subjects was approximately 3.8 μmol kg −1 min −1 . If a correction factor (for label dilution in the tricarboxylic acid cycle) of ∼1.5 is used [20], gluconeogenesis is 70% of EGP (8.1 μmol kg −1 min −1…”

Section: Such a Cyclic State Which Is Then Necessarily Restrictedmentioning

confidence: 99%

Diurnal rhythm in endogenous glucose production is a major contributor to fasting hyperglycaemia in type 2 diabetes. Suprachiasmatic deficit or limit cycle behaviour?

Radziuk

Pye

2006

Diabetologia

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Aims/hypothesis: An increase in endogenous glucose production (EGP) is a major contributor to fasting morning hyperglycaemia in type 2 diabetes. This increase is dissipated with fasting, later in the day. To understand its origin, EGP, gluconeogenesis and hormones that regulate metabolism were measured over 24 h. We hypothesised that EGP, and therefore glycaemia, would demonstrate a centrally mediated circadian rhythm in type 2 diabetes. Subjects and methods: Seven subjects with type 2 diabetes and six age-and BMI-matched control subjects, fasting after breakfast (08

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Correction for metabolic exchange in the calculation of the rate of gluconeogenesis in rats

Cited by 45 publications

References 9 publications

Quantitative analysis of glycogen repletion by nuclear magnetic resonance spectroscopy in the conscious rat.

Quantitative analysis of glycogen repletion by nuclear magnetic resonance spectroscopy in the conscious rat.

Postprandial hyperglycemia in patients with noninsulin-dependent diabetes mellitus. Role of hepatic and extrahepatic tissues.

Diurnal rhythm in endogenous glucose production is a major contributor to fasting hyperglycaemia in type 2 diabetes. Suprachiasmatic deficit or limit cycle behaviour?

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