Regulation of Inflammation by Sucrose Isomer, Turanose, in Raw 264.7 Cells

Increased sugar consumption has been proposed to be a risk factor for obesity-related metabolic disorders. The objective of this study was to investigate the anti-inflammatory effect of turanose in Raw 264.7 macrophages. Turanose (3-O-α-D-glucosyl-D-fructose), an isomer of sucrose, naturally exists in honey. For these studies, macrophages were treated with total glucose (Glu), 50% Glu/50% turanose (T50), 25% Glu/75% turanose (T75), and 100% turanose (T100), each with a total concentration of 25 mM in cell media. Expressions of inflammatory enzymes and cytokines were analyzed. Cell viability was not affected in the turanose treated groups compared to the Glu group. Lipopolysaccharide and glucose-induced nitric oxide production, protein expression of inducible nitric oxide synthase, COX-2, and superoxide dismutase 2, and mRNA expression levels of interleukin (IL)-1β and IL-18 were significantly suppressed by turanose treatment. These results demonstrate that turanose exerts anti-inflammatory effects in vitro, and possesses potential to serve therapeutic functional sweetener for testing in vivo and in clinical trials.

Acute and 13-week subchronic toxicological evaluations of turanose in mice

BACKGROUND/OBJECTIVES: Turanose, α-D-glucosyl-(1→3)-α-D-fructose, is a sucrose isomer which naturally exists in honey. To evaluate toxicity of turanose, acute and subchronic oral toxicity studies were conducted with ICR mice. MATERIALS AND METHODS: For the acute oral toxicity study, turanose was administered as a single oral dose [10 g/kg body weight (b.w.)]. In the subchronic toxicity study, ICR mice were administered 0, 1.75, 3.5, and 7 g/kg b.w. doses of turanose daily for 13 weeks. RESULTS: No signs of acute toxicity, including abnormal behavior, adverse effect, or mortality, were observed over the 14-day study period. In addition, no changes in body weight or food consumption were observed and the median lethal dose (LD₅₀) for oral intake of turanose was determined to be greater than 10 g/kg b.w. General clinical behavior, changes in body weight and food consumption, absolute and relative organ weights, and mortality were not affected in any of the treatment group for 13 weeks. These doses also did not affect the macroscopic pathology, histology, hematology, and blood biochemical analysis of the mice examined. CONCLUSION: No toxicity was observed in the acute and 13-week subchronic oral toxicology studies that were conducted with ICR mice. Furthermore, the no-observed-adverse-effect level is greater than 7 g/kg/day for both male and female ICR mice.