The objective of this study is to investigate the effects of vitamin A, D and their interaction on the glycaemic control in patients with both diabetes and tuberculosis. Tuberculosis infection and its treatment induce hyperglycaemia and complicate the glycaemic control in patients with diabetes. A randomised controlled trial with a 2 × 2 factorial design was conducted in a tuberculosis-specialised hospital in Qingdao, China. A total of 279 patients who have both diabetes and tuberculosis were included in this analysis. The patients received standard anti-tuberculosis treatment alone (control group), or together with a dose of vitamin A (600 μg RAE/d) or vitamin D (10 μg/d) or a combination of vitamin A (600 μg RAE/d) and vitamin D (10 μg/d) for 2 months. The effects of the intervention on fasting plasma glucose and 2-h postprandial blood glucose were investigated by ANCOVA. The analysis was adjusted for baseline values, age, sex, smoking, drinking and antidiabetic treatment as covariates. No significant effect was observed for vitamin A and D supplementation on fasting plasma glucose, 2-h postprandial blood glucose, BMI and related blood parameters. No interaction was observed between vitamin A and D supplementation for these endpoints. Vitamin A and D supplementation showed a null effect on the glycaemic control for patients with concurrent diabetes and tuberculosis. Future work should evaluate the effect of vitamin A and D supplementation on insulin-related indices for these patients and investigate the effect of vitamin D receptor genotypes.

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.