The inhibition by 1,5-anhydro-d-glucitol (1,5-AG) was determined on disaccharidases of rats and humans. Then, the metabolism and fate of 1,5-AG was investigated in rats and humans. Although 1,5-AG inhibited about 50 % of sucrase activity in rat small intestine, the inhibition was less than half of d-sorbose. 1,5-AG strongly inhibited trehalase and lactase, whereas d-sorbose inhibited them very weakly. 1,5-AG noncompetitively inhibited sucrase. The inhibition of 1,5-AG on sucrase and maltase was similar between humans and rats. 1,5-AG in serum increased 30 min after oral administration of 1,5-AG (600 mg) in rats, and mostly 100 % of 1,5-AG was excreted into the urine 24 h after administration. 1,5-AG in serum showed a peak 30 min after ingestion of 1,5-AG (20 g) by healthy subjects, and decreased gradually over 180 min. About 60 % of 1,5-AG was excreted into the urine for 9 h following ingestion. Hydrogen was scarcely excreted in both rats and humans 24 h after administration of 1,5-AG. Furthermore, 1,5-AG significantly suppressed the blood glucose elevation, and hydrogen excretion was increased following the simultaneous ingestion of sucrose and 1,5-AG in healthy subjects. 1,5-AG also significantly suppressed the blood glucose elevation following the simultaneous ingestion of glucose and 1,5-AG; however, hydrogen excretion was negligible. The available energy of 1,5-AG, which is absorbed readily from the small intestine and excreted quickly into the urine, is 0 kJ/g (0 kcal/g). Furthermore, 1,5-AG might suppress the blood glucose elevation through the inhibition of sucrase, as well as intestinal glucose absorption.
Keywords: 1; BBMV brush border membrane vesicles; FOS fructo-oligosaccharide; 1; 5-AF 1; 5-AG 1; 5-Anhydro-d-glucitol; 5-Anhydroglucitol; 5-anhydro-d-fructose; 5-anhydro-d-glucitol; Disaccharidase; Hydrogen excretion; Postprandial blood glucose.