Research Paper Volume 12, Issue 14 pp 13991—14018

Peanut skin extract ameliorates the symptoms of type 2 diabetes mellitus in mice by alleviating inflammation and maintaining gut microbiota homeostasis

Lan Xiang1, , Qiaobei Wu1, , Hiroyuki Osada2, , Minoru Yoshida3,4, , Wensheng Pan5, , Jianhua Qi1, ,

  • 1 College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, P. R. China
  • 2 Chemical Biology Research Group, RIKEN Center for Sustainable Resource Science, Wako-Shi, Saitama, Japan
  • 3 Chemical Genomics Research Group, RIKEN Center for Sustainable Resource Science, Wako, Saitama, Japan
  • 4 Department of Biotechnology and Collaborative Research Institute for Innovative Microbiology, The University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • 5 Department of Gastroenterology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang Province, China

Received: March 27, 2020       Accepted: June 5, 2020       Published: July 22, 2020
How to Cite

Copyright © 2020 Xiang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


In this study, mice with type 2 diabetes mellitus (T2DM) induced by high-fat diet were used to investigate the antidiabetic effect and mechanism of action of peanut skin extract (PSE). Results revealed that the fasting blood glucose, body weight, and food intake of mice with T2DM significantly decreased after they were given PSE. The effects of 80 mg/kg PSE were similar to those of 140 mg/kg metformin (MET). The glucose tolerance and insulin sensitivity of the mice also improved. The composition of intestinal microflora in the mice significantly changed after PSE administration. In particular, no Actinobacteria was detected in the PSE-treated group, and the ratio of Firmicutes to Bacteroidetes was remarkably reduced. PSE also increased the abundance of gut microbiota involved in fatty acid biosynthesis, lipid biosynthesis, and sucrose metabolism. The abundance of gut microbiota related to aminoacyl-tRNA biosynthesis also decreased. Lipopolysaccharide, interleukin (IL)-6, IL-1β and tumor necrosis factor-α in the blood, liver and adipose tissue were reduced by PSE. Similarly, the mRNA expression levels of IkappaB kinase and nuclear factor kappaB in the hypothalamus were reduced by PSE. These results suggested that PSE and MET elicited significant antidiabetic effects by maintaining gut microbiota and inhibiting inflammation.


ALT: Alanine aminotransferase; AST: Aspartate aminotransferase ; AUC: Area under the curve; COG: Clusters of orthologous groups; DM: Diabetic model control group; FDR: False discovery rate; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; GnRH: Gonadotropin-releasing hormone; HDL: High-density lipoprotein; HFD: High fat diet; HPLC: High Performance Liquid Chromatography; ITT: Insulin tolerance test; ICR: Institute for Cancer Research; IKK-β: IkappaB kinase; IL-6: Interleukin-6; JAK2: Janus kinase 2; KEGG: Kyoto Encyclopedia of Genes and Genomes; LDA: Linear Discriminant Analysis; LEFSE: LDA Effect Size; LPS: Lipopolysaccharide; MET: Metformin; ND: normal diet; NF-Kβ: Nuclear factor kB; OGTT: Oral Glucose Tolerance Tests; PSE: Peanut skin extract; PICRUST: Phylogenetic Investigation of Communities by Reconstruction of Unobserved States; SOCS3: Suppressors of cytokine signaling 3; STAT3: Signal transducer and activator of transcription 3; SEM: Standard error of the mean; TC: total cholesterol; TG: Triglycerides; T2DM: Type 2 diabetes mellitus.