Abstract
PURPOSE OF REVIEW: The rise in fructose consumption in parallel with the current epidemic of obesity and related cardiometabolic disease requires a better understanding of the pathophysiological pathways that are involved.
RECENT FINDINGS: Animal studies have shown that fructose has various effects on the intestines that subsequently affect intrahepatic lipid accumulation and inflammation. Fructose adversely affects the gut microbiome - as a producer of endotoxins and intermediates of de novo lipogenesis - and intestinal barrier function. Furthermore, intestinal fructose metabolism shields fructose away from the liver. Finally, fructose 1-phosphate (F1-P) serves as a signal molecule that promotes intestinal cell survival and, consequently, intestinal absorption capacity. Intervention and epidemiological studies have convincingly shown that fructose, particularly derived from sugar-sweetened beverages, stimulates de novo lipogenesis and intrahepatic lipid accumulation in humans. Of interest, individuals with aldolase B deficiency, who accumulate F1-P, are characterized by a greater intrahepatic lipid content. First phase II clinical trials have recently shown that reduction of F1-P, by inhibition of ketohexokinase, reduces intrahepatic lipid content.
SUMMARY: Experimental evidence supports current measures to reduce fructose intake, for example by the implementation of a tax on sugar-sweetened beverages, and pharmacological inhibition of fructose metabolism to reduce the global burden of cardiometabolic disease.
Original language | English |
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Pages (from-to) | 354-359 |
Number of pages | 6 |
Journal | Current Opinion in Clinical Nutrition and Metabolic Care |
Volume | 25 |
Issue number | 5 |
Early online date | 16 Jul 2022 |
DOIs | |
Publication status | Published - Sept 2022 |
Keywords
- DIETARY FRUCTOSE
- GLUCOKINASE
- GLUCOSE
- INHIBITION
- KETOHEXOKINASE
- LIPOGENESIS
- LIVER FAT
- MICROBIOTA
- SUGAR
- aldolase B
- colorectal cancer
- fructose
- ketohexokinase
- nonalcoholic fatty liver disease