On the inhibition of hepatic glycogenolysis by fructose. A31P-NMR study in perfused rat liver using the fructose analogue 2,5-anhydro-D-mannitol

Bruynseels, Koen; Bergans, Niki; Gillis, N; Dorpen, F van; Hecke, Paul Van; Stalmans, Willy; Vanstapel, Florent

doi:10.1002/(sici)1099-1492(199905)12:3<145::aid-nbm559>3.0.co;2-1

Cited by 7 publications

References 45 publications

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Fructose, uricase, and the Back‐to‐Africa hypothesis

Johnson

Andrews

2010

Evolutionary Anthropology

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In the Middle Miocene (approximately 17 to 12 Ma) at least two radiations of fossil apes from East Africa into Eurasia occurred, and, while controversial, some paleoanthropological studies suggest that one of the Eurasian lineages may have returned to Africa to evolve into humans and the African apes. Here, we present a novel argument supporting this hypothesis. Specifically, the global cooling that occurred in the middle Miocene rendered hominoids living in Europe at risk for starvation as seasonal climate change resulted in less availability of fruits during the winter months. During this time, a mutation in uricase occurred in early hominids that resulted in a rise in serum uric acid. Uric acid has been found to potentiate the effect of fructose to increase fat stores, suggesting that the mutation provided a survival advantage. Such a survival advantage would have been less likely to occur in Africa, where the continued presence of tropical rainforests would have been more likely to provide food throughout the year. Furthermore, Miocene apes in Europe were in protected sites where geographic isolation could have allowed the uricase mutation to be rapidly expressed in the entire population. While speculative, we suggest that the uricase mutation supports an extra‐Africa origin of humans.

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Fructose, uricase, and the Back‐to‐Africa hypothesis

Johnson

Andrews

2010

Evolutionary Anthropology

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Quantification of the glycogen ¹³C‐1 NMR signal during glycogen synthesis in perfused rat liver

et al. 2003

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We studied glycogen synthesis from glucose in perfused livers of fed (n = 4) and 24 h starved (n = 7) rats. Glycogenolysis was inhibited by BAY R3401 (150 microM) and proglycosyn (100 microM). After 60 min, we replaced 99% (13)C-1 glucose by natural abundance glucose. This pulse-chase design allowed us to recognize residual ongoing futile glycogen turnover from the release of initially deposited (13)C-label, into the (13)C-free chase medium. Net residual turnover was less than 2 +/- 0.7% and 0.6 +/- 0.2% of 1-(13)C glycogen deposition rates of 0.31 +/- 0.04 and 0.99 +/- 0.04 micromol glucose g(-1) min(-1), in starved and fed livers, respectively. The 1-(13)C glycogen signal was monitored throughout the experiment with proton-decoupled (13)C NMR spectroscopy and analyzed in the time domain using AMARES. We noticed progressive line-broadening in any single experiment in the chase phase. One or a sum of two to three overlapping Lorentzians, with different exponential damping factors, were fitted to the signal. When the S/N was better than 40, the fit always delivered a small and a broad component. In the chase phase, the fit with a single Lorentzian resulted in a decline of glycogen signal by about 15 +/- 4 and 12 +/- 2% in starved and fed rats, respectively. This apparent decline in 1-(13)C glycogen signal could not be accounted for by the appearance of equivalent amounts of (13)C-labeled metabolites in the perfusate. The fit with a sum of two Lorentzians resulted in a decline of glycogen signal intensity of 7 +/- 5 and 5 +/- 3% in starved and fed rats, respectively, which reduced the apparent turnover to 8 +/- 9% and 6 +/- 4%, respectively. Quantification of the growing (13)C-1 glycogen signal requires a model function that accommodates changes in line shape throughout the period under study.

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Biomedicine of Monosaccharides

Osborn¹,

Evans²,

Bezouška³

2008

Glycoscience

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On the inhibition of hepatic glycogenolysis by fructose. A31P-NMR study in perfused rat liver using the fructose analogue 2,5-anhydro-D-mannitol

Cited by 7 publications

References 45 publications

Fructose, uricase, and the Back‐to‐Africa hypothesis

Fructose, uricase, and the Back‐to‐Africa hypothesis

Quantification of the glycogen ¹³C‐1 NMR signal during glycogen synthesis in perfused rat liver

Biomedicine of Monosaccharides

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On the inhibition of hepatic glycogenolysis by fructose. A31P-NMR study in perfused rat liver using the fructose analogue 2,5-anhydro-D-mannitol

Cited by 7 publications

References 45 publications

Fructose, uricase, and the Back‐to‐Africa hypothesis

Fructose, uricase, and the Back‐to‐Africa hypothesis

Quantification of the glycogen 13C‐1 NMR signal during glycogen synthesis in perfused rat liver

Biomedicine of Monosaccharides

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Product

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Quantification of the glycogen ¹³C‐1 NMR signal during glycogen synthesis in perfused rat liver