Anti-Diabetic Effects of Allulose in Diet-Induced Obese Mice via Regulation of mRNA Expression and Alteration of the Microbiome Composition

Nutrients. 2020 Jul 16;12(7):2113. doi: 10.3390/nu12072113.


Allulose has been reported to serve as an anti-obesity and anti-diabetic food component; however, its molecular mechanism is not yet completely understood. This study aims to elucidate the mechanisms of action for allulose in obesity-induced type 2 diabetes mellitus (T2DM), by analyzing the transcriptional and microbial populations of diet-induced obese mice. Thirty-six C57BL/6J mice were divided into four groups, fed with a normal diet (ND), a high-fat diet (HFD), a HFD supplemented with 5% erythritol, or a HFD supplemented with 5% allulose for 16 weeks, in a pair-fed manner. The allulose supplement reduced obesity and comorbidities, including inflammation and hepatic steatosis, and changed the microbial community in HFD-induced obese mice. Allulose attenuated obesity-mediated inflammation, by downregulating mRNA levels of inflammatory response components in the liver, leads to decreased plasma pro-inflammatory marker levels. Allulose suppressed glucose and lipid metabolism-regulating enzyme activities, ameliorating hepatic steatosis and improving dyslipidemia. Allulose improved fasting blood glucose (FBG), plasma glucose, homeostatic model assessment of insulin resistance (HOMA-IR), and the area under the curve (AUC) for the intraperitoneal glucose tolerance test (IPGTT), as well as hepatic lipid levels. Our findings suggested that allulose reduced HFD-induced obesity and improved T2DM by altering mRNA expression and the microbiome community.

Keywords: anti-diabetes; anti-obesity; functional sweetener; rare sugar.

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / etiology
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / microbiology*
  • Diabetes Mellitus, Type 2 / therapy*
  • Diet, High-Fat / adverse effects*
  • Dietary Supplements*
  • Fructose / administration & dosage*
  • Fructose / pharmacology
  • Gastrointestinal Microbiome*
  • Glucose / metabolism
  • Hypoglycemic Agents*
  • Inflammation
  • Inflammation Mediators / metabolism
  • Insulin Resistance
  • Lipid Metabolism
  • Liver / metabolism
  • Male
  • Mice, Inbred C57BL
  • Obesity / etiology
  • Obesity / metabolism
  • Obesity / microbiology*
  • Obesity / therapy*
  • Phytotherapy*
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism*


  • Hypoglycemic Agents
  • Inflammation Mediators
  • RNA, Messenger
  • psicose
  • Fructose
  • Glucose