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1.
Figure 3

Figure 3. From: Alterations in Hepatic Glucose and Energy Metabolism as a Result of Calorie and Carbohydrate Restriction.

Relationship Between PEPCK Flux and TCA Cycle Flux.

Jeffrey D. Browning, et al. Hepatology. ;48(5):1487-1496.
2.
Figure 1

Figure 1. From: Alterations in Hepatic Glucose and Energy Metabolism as a Result of Calorie and Carbohydrate Restriction.

2H-NMR Analysis of the Incorporation of Deuterium Oxide into Glucose. Protons derived from water are incorporated into glucose at three distinct steps of its production. After enrichment of total body water by oral ingestion of deuterium oxide (2H2O), deuterons are incorporated into glucose via the same mechanism. All glucose produced, whether from gluconeogenesis or from glycogenolysis, becomes enriched at carbon 2 of glucose (H2). All glucose derived from gluconeogenesis becomes enriched at carbon 5 of glucose (H5) while only gluconeogenesis occurring from precursors originating in the TCA cycle (PEP) becomes enriched at carbon 6s of glucose (H6s). The relative enrichment of deuterium at each of the carbon positions of glucose, after conversion to its monoacetone derivative, is easily discerned by computing the peak areas obtained by 2H-NMR spectroscopy. The ratio of H5/H2 gives the proportion of glucose that is derived from gluconeogenesis while (H5-H6s)/H2 gives the proportion of glucose derived from PEP. The H5/H2 ratio of the two depicted spectra are quite different: the low-calorie spectra indicates that gluconeogenesis accounts for ∼50% of glucose production while the low-carbohydrate spectra indicates that ∼80% of glucose is derived from gluconeogenesis.

Jeffrey D. Browning, et al. Hepatology. ;48(5):1487-1496.
3.
Figure 2

Figure 2. From: Alterations in Hepatic Glucose and Energy Metabolism as a Result of Calorie and Carbohydrate Restriction.

13C-NMR Analysis of the Incorporation of [U-13C]propionate into Glucose. After ingestion, propionate is avidly taken up by liver and enters the TCA cycle as [1,2,3-13]succinyl-CoA. Within the TCA cycle, this labeled intermediate can have one of three fates: 1) exit the TCA cycle as phosphoenolpyruvate (PEP) immediately upon conversion to oxaloacetate (OAA) via the action of phosphoenolpyruvate carboxykinase (PEPCK), ultimately leading to the formation of [1,2,3-13C]glucose and [1,2-13C]glucose in a 1:1 proportion; 2) proceed through a complete turn of the TCA cycle, passing through citrate synthase, and exiting the cycle as PEP, ultimately yielding [2-13C]glucose and [2,3-13C]glucose; and 3) exit the TCA cycle as PEP with subsequent conversion from PEP to pyruvate to OAA and back to PEP (so-called pyruvate cycling), ultimately leading to the formation of [1,2,3-13C]glucose and [1,2-13C]glucose in a 1:3 proportion. By examining the C2 of glucose using 13C-NMR after conversion to its monoacetone derivative, each of these glucose isotopomers is readily apparent: [1,2,3-13C]glucose is denoted in the spectrum by the quartet (Q); [2,3-13C]glucose is represented by the doublet D23; [1,2-13C]glucose is represented by the doublet D12; and [2-13C]glucose is represented by the singlet peak in the center of the C2 spectrum (not labeled). The areas under each of these peaks provides the information necessary to calculate PEPCK flux, pyruvate cycling, and the rate of production GNGPEP relative to citrate synthase flux. These pathways and the isotopomers they produced can also be described by a full set of analytical equations (24).

Jeffrey D. Browning, et al. Hepatology. ;48(5):1487-1496.

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