Fructose and metabolic health

governed by hepatic glycogen status?

Research output: Contribution to journalReview article

1 Citation (Scopus)

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 rationale for considering nutrient‐physical activity interactions in metabolic health.
Original languageEnglish
Pages (from-to)1-13
Number of pages13
JournalThe Journal of Physiology
Early online date5 Apr 2019
DOIs
Publication statusE-pub ahead of print - 5 Apr 2019

Keywords

  • fructose
  • liver
  • hepatic
  • glycogen
  • de novo lipogenesis
  • metabolism

Cite this

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title = "Fructose and metabolic health: governed by hepatic glycogen status?",
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 rationale for considering nutrient‐physical activity interactions in metabolic health.",
keywords = "fructose, liver, hepatic, glycogen, de novo lipogenesis, metabolism",
author = "Aaron Hengist and Francoise Koumanov and Javier Gonzalez",
year = "2019",
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journal = "Journal of Physiology",
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TY - JOUR

T1 - Fructose and metabolic health

T2 - governed by hepatic glycogen status?

AU - Hengist, Aaron

AU - Koumanov, Francoise

AU - Gonzalez, Javier

PY - 2019/4/5

Y1 - 2019/4/5

N2 - 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 rationale for considering nutrient‐physical activity interactions in metabolic health.

AB - 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 rationale for considering nutrient‐physical activity interactions in metabolic health.

KW - fructose

KW - liver

KW - hepatic

KW - glycogen

KW - de novo lipogenesis

KW - metabolism

U2 - 10.1113/JP277767

DO - 10.1113/JP277767

M3 - Review article

SP - 1

EP - 13

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

ER -