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Abstract
Fructose is a commonly ingested dietary sugar which has been implicated in playing a particularly harmful role in the development of metabolic disease. Fructose is primarily metabolised by the liver in humans, and increases rates of hepatic de novo lipogenesis. Fructose increases hepatic de novo lipogenesis via numerous mechanisms: by altering transcriptional and allosteric regulation, interfering with cellular energy sensing, and disrupting the balance between lipid synthesis and lipid oxidation. Hepatic de novo lipogenesis is also upregulated by the inability to synthesise glycogen, either when storage is inhibited in knock-down animal models or storage is saturated in glycogen storage disease. Considering that fructose has the capacity to upregulate hepatic glycogen storage, and replenish these stores more readily following glycogen depleting exercise, the idea that hepatic glycogen storage and hepatic de novo lipogenesis are linked is an attractive prospect. We propose that hepatic glycogen stores may be a key factor in determining the metabolic responses to fructose ingestion, and saturation of hepatic glycogen stores could exacerbate the negative metabolic effects of excessive fructose intake. Since physical activity potently modulates glycogen metabolism, this provides a rationale for considering nutrient-physical activity interactions in metabolic health.
Original language | English |
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Pages (from-to) | 3573-3585 |
Number of pages | 13 |
Journal | The Journal of Physiology |
Volume | 597 |
Issue number | 14 |
Early online date | 5 Apr 2019 |
DOIs | |
Publication status | Published - 15 Jul 2019 |
Bibliographical note
© 2019 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.Keywords
- fructose
- liver
- hepatic
- glycogen
- de novo lipogenesis
- metabolism
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Dive into the research topics of 'Fructose and metabolic health: governed by hepatic glycogen status?'. Together they form a unique fingerprint.Projects
- 1 Finished
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Role of Rab3 in Peripheral Tissue Insulin Resistance
Koumanov, F. (PI), Betts, J. (CoI), Gonzalez, J. (CoI), Thompson, D. (CoI) & Whitley, P. (CoI)
1/12/16 → 31/07/20
Project: Research council