Glucose-sensing transcription factor mondoa/chrebp as targets for type 2 diabetes: Opportunities and challenges

Ziyi Song, Hao Yang, Lei Zhou, Fajun Yang

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


The worldwide increase in type 2 diabetes (T2D) is becoming a major health concern, thus searching for novel preventive and therapeutic strategies has become urgent. In last decade, the paralogous transcription factors MondoA and carbohydrate response element-binding protein (ChREBP) have been revealed to be central mediators of glucose sensing in multiple metabolic organs. Under normal nutrient conditions, MondoA/ChREBP plays vital roles in maintaining glucose homeostasis. However, under chronic nutrient overload, the dysregulation of MondoA/ChREBP contributes to metabolic disorders, such as insulin resistance (IR) and T2D. In this review, we aim to provide an overview of recent advances in the understanding of MondoA/ChREBP and its roles in T2D development. Specifically, we will briefly summarize the functional similarities and differences between MondoA and ChREBP. Then, we will update the roles of MondoA/ChREBP in four T2D-associated metabolic organs (i.e., the skeletal muscle, liver, adipose tissue, and pancreas) in physiological and pathological conditions. Finally, we will discuss the opportunities and challenges of MondoA/ChREBP as drug targets for anti-diabetes. By doing so, we highlight the potential use of therapies targeting MondoA/ChREBP to counteract T2D and its complications.

Original languageEnglish (US)
Article number5132
JournalInternational Journal of Molecular Sciences
Issue number20
StatePublished - Oct 2 2019


  • Adipose tissue
  • ChREBP
  • Glucose
  • Insulin resistance
  • Liver
  • Metabolism
  • MondoA
  • Pancreas
  • Skeletal muscle
  • Type 2 diabetes

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry


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