Xylobiose ameliorates hyperglycemia and dyslipidemia via regulating hepatic lipogenic genes in db/db mice

Abstract

Diabetes mellitus (DM) is a metabolic disorder in glucose and fat metabolism and has become a major public concern in worldwide. Xylobiose consists of two molecules of xylose and is a major disaccharide in a well‐known sweetener, xylo‐oligosaccharide. Although it has been reported the hypoglycemic effect of xylo‐oligosaccharide, the physiological effect of xylobiose on blood glucose and lipogenesis has not been evaluated. The objective of study was to evaluate the hypoglycemic and hypolipogenic effect of xylobiose in db/db mice. Five‐ week old male C57BL/KsJ‐db/db mice were randomized into 3 groups as follows: (1) a control group of C57BL/6 mice that received AIN93G (Ctrl), (2) a diabetic control group of C57BL/KsJ‐db/db mice that received AIN93G (DB), and (3) a group that supplemented with 5% xylobiose as part of the total sucrose content of the diet (XB5). Mice were fed the experimental diets for 6 weeks. Supplementation of xylobiose reduced food and water intake and improved glucose tolerance by reducing the levels of oral glucose tolerance test area under the curve, fasting blood glucose, HbA1c, insulin, and HOMA‐IR. These results indicate xylobiose attenuates hyperglycemia by regulating insulin and blood glucose metabolism. In addition, xylobiose supplementation significantly decreased the levels of TG, total cholesterol, and LDL‐C. Histopathologically, fat accumulation in liver tissues was reduced in XB 5 group. Expressions of lipogenic genes, including, FAS, PPARγ, SREBP‐1C, SREBP‐2, ACC, and HMG‐CoA reductase in liver tissues were significantly down‐regulated by xylobiose supplementation. Furthermore, xylobiose supplementation suppressed the mRNA expressions of pro‐inflammatory cytokines, TNF‐α, IL‐1β, IL‐6, and MCP‐1 and phosphorylation of three MAPK, such as JNK/SAPK, p38, and ERK (1/2). Taken together, xylobiose exhibits considerable anti‐diabetic, hypolipogenic, and anti‐inflammatory alternation in db/db mice.Support or Funding InformationThis research was supported by High Value‐added Food Technology Development Program (Project number: 313024‐03‐2‐HD040), Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea, and Brain Korea 21 Plus (Project No. 22A20130012143)