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Fructose metabolism: The pathogenic potential of a little molecule

Dijana Mirić Orcid logo ,
Dijana Mirić
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Bojana Kisić Orcid logo ,
Bojana Kisić
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Dragana Pavlović ,
Dragana Pavlović
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Ilija Dragojević Orcid logo ,
Ilija Dragojević
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Sladoje Puhalo
Sladoje Puhalo
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Published: 01.12.2021.

Volume 51, Issue 3 (2022)

pp. 45-52;

https://doi.org/10.5937/pramed2204045m

Abstract

In recent decades, the use of fructose in diet has increased worldwide, and coincided with increase of obesity, metabolic syndrome, diabetes, and non-alcoholic liver disease. This review presents molecular aspects of fructose metabolism, its characteristics and contemporary knowledge about control mechanisms in order to answer how this small molecule can exert pathogenic effects. When present in small, physiological amounts, fructose actually exerts protective glycoregulatory effects. However, long-term exposure to supraphysiological amounts of fructose creates conditions for the development of certain pathological states. In such conditions, lipogenesis is intensified causing dyslipidemia, gluconeogenesis is also intensified leading to hyperglycemia and compensatory hyperinsulinemia, while insulin signaling through IP3K/Akt is blocked. Moreover, exposure to high fructose levels can induce inflammation, redox balance disruption and a decline in energy synthesis. It is most likely that the ability of the liver to metabolize large amounts of fructose and the absence of autoregulatory and hormonal control mechanisms are responsible for pathogenic potential of fructose.

References

1.
Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, et al. A causal role for uric acid in fructose-induced metabolic syndrome. American Journal of Physiology-Renal Physiology. 2006;290(3):F625–31.
2.
GIBSON PR, NEWNHAM E, BARRETT JS, SHEPHERD SJ, MUIR JG. Review article: fructose malabsorption and the bigger picture. Alimentary Pharmacology & Therapeutics. 2007;25(4):349–63.
3.
Jang C, Hui S, Lu W, Cowan AJ, Morscher RJ, Lee G, et al. The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids. Cell Metabolism. 2018;27(2):351-361.e3.
4.
Yu S, Li C, Ji G, Zhang L. The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease. Frontiers in Pharmacology. 12.
5.
Guney C, Bal NB, Akar F. The impact of dietary fructose on gut permeability, microbiota, abdominal adiposity, insulin signaling and reproductive function. Heliyon. 2023;9(8):e18896.

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