Abstract

D‐allulose is found in a wide variety of food products in limited amounts, and therefore is referred to as a rare sugar. It is an epimer of fructose that is 70% as sweet as sucrose and has been demonstrated to have antihyperglycemic, antihyperlipidemic, and antiobesity effects by various studies including humans. The mechanism underlying intestinal absorption of D‐allulose is unknown, hence we tested the hypothesis that intestinal D‐allulose transport is mediated by glucose transporter type 5 (GLUT5). Adult rats were initially fed for a week a high‐fructose (control: high‐glucose) diet to induce GLUT5 expression and then gavaged with 1g/kg BW D‐allulose alone, D‐allulose with 1g/kg BW glucose or D‐allulose with 1g/kg BW fructose. Plasma D‐allulose concentrations were then compared to examine whether D‐allulose shares transporters with fructose and/or glucose and whether its absorption is affected by luminal glucose or fructose. When D‐allulose was gavaged alone, the fructose‐fed rats showed significantly higher plasma D‐allulose levels at 30, 60, 90 min and conversely lower (P = 0.05) level at 120 min after administration than those of the glucose‐fed rats. This suggests that more D‐allulose was rapidly absorbed via highly expressed GLUT5 in the fructose‐fed rats. When D‐allulose was gavaged with fructose, appearance of D‐allulose in the plasma was delayed compared to when D‐allulose alone was administrated, indicating that fructose inhibited D‐allulose transport into plasma. Moreover, the levels of plasma fructose peaked earlier than those of D‐allulose, indicating that luminal fructose is more rapidly absorbed than D‐allulose. When D‐allulose was gavaged with glucose, higher plasma D‐allulose concentrations at 30 min after administration were observed compared to when D‐allulose was gavaged with fructose in both glucose‐ and fructose‐fed rats. These results suggest that intestinal D‐allulose transport is likely mediated by GLUT5 and its affinity for GLUT5 is lower than that of fructose.Support or Funding InformationThis work was partly supported by Matsutani Chemical Industry Co., Ltd.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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