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dimanche 17 février 2013

Dysnutrition and cancer: the case of fructose in pancreatic cancer

Images intégrées 1
Figure 5. Schematic model summarizing the differences in glucose (A) and fructose (B) metabolism in pancreatic cancer cells showing the preferential use of  fructose in the TK-dependent nonoxidative pentose phosphate shunt. 

Cancer Res; 70(15) August 1, 2010

And more recently:
"Fructose intake has increased dramatically since humans were hunter-gatherers, probably outpacing the capacity of human evolution to make physiologically healthy adaptations. Epidemiological data indicate that this increasing trend continued until recently. Excessive intakes that chronically increase portal and peripheral blood fructose concentrations to >1 and 0.1 mM, respectively, are now associated with numerous diseases and syndromes."

Figure 8 Schematic model of Glut5 regulation in small intestinal cells of 20-day-old pups
Age-related increases in corticosterone levels lead to binding with and dimerization of the GR in the cytosol, which then translocate to the nuclei and simultaneously stimulate modest levels of histone H3 acetylation. This step is required for Glut5 regulation as fructose is unable to stimulate Glut5 in 10-day-old rats without the GR in the nuclei. Injecting 10-day-old rats with the glucocorticoid analogue dexamethasone relieves the age-related inhibition of Glut5 by fructose [13]. Perfusion with fructose leads to recruitment of unknown transcription factors (TF) which have HAT activity, thereby increasing the magnitude of age-related increases in histone H3 acetylation in the Glut5 promoter.

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