Oral recombinant methioninase inhibits diabetes onset in mice on a high-fat diet

Yoshihiko Tashiro, Qinghong Han, Yuying Tan, Norihiko Sugisawa, Jun Yamamoto, Hiroto Nishino, Sachiko Inubushi, Yu Sun, Guangwei Zhu, Hyein Lim, Takeshi Aoki, Masahiko Murakami, Michael Bouvet, Robert M. Hoffman

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Background/Aim: We have recently shown that oral recombinant methionase (o-rMETase) prevents obesity in mice on a high-fat (HF) diet. The present study aimed to determine if o-rMETase can inhibit the onset of diabetes in mice on a HF diet. Materials and Methods: The mice on a HF diet were divided into two groups: 1) HF+phosphate buffered saline (PBS) group; 2) HF+o-rMETase group. Results: The blood glucose level in the HF+PBS group increased to average of 201 mg/dl during the experimental period of 8 weeks. In contrast, the blood glucose level in the HF+o-rMETase group maintained an average of 126 mg/dl (p<0.01, HF+PBS vs. HF+o-rMETase). The glucose tolerance test showed a significant increase in tolerance in the HF+o-rMETase group at 120 min after glucose injection compared to the HF+PBS group (p=0.04). Visceral adipose tissue was significantly less in the HF+o-rMETase group than the HF+PBS group (p=0.05). There was no difference in insulin levels, cholesterol or triglycerides between the HF+PBS and HF+o-rMETase groups. Conclusion: o-rMETase inhibited the onset of diabetes as well as prevented obesity on a high-fat diet, offering a possibility of a new and easy-to-use alternative to severe dieting or insulin injections.

Original languageEnglish
Pages (from-to)973-978
Number of pages6
JournalIn Vivo
Issue number3
Publication statusPublished - 2020 Jun
Externally publishedYes


  • Diabetes
  • High-fat diet
  • MR
  • Methioninase
  • Methionine restriction
  • Mice

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology


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