Abstract |
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.
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Authors | Ziyi Song, Hao Yang, Lei Zhou, Fajun Yang |
Journal | International journal of molecular sciences
(Int J Mol Sci)
Vol. 20
Issue 20
(Oct 16 2019)
ISSN: 1422-0067 [Electronic] Switzerland |
PMID | 31623194
(Publication Type: Journal Article, Review)
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Chemical References |
- Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
- Biomarkers
- Insulin
- MLXIP protein, human
- MLXIPL protein, human
- Glucose
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Topics |
- Adipose Tissue
(drug effects, metabolism)
- Animals
- Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
(genetics, metabolism)
- Biomarkers
- Diabetes Mellitus, Type 2
(drug therapy, etiology, metabolism)
- Gene Expression Regulation
- Glucose
(metabolism)
- Humans
- Insulin
(metabolism)
- Insulin Resistance
- Liver
(metabolism)
- Pancreas
(metabolism)
- Signal Transduction
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