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Review
.2023 May 16;24(10):8811.
doi: 10.3390/ijms24108811.

The Function of MondoA and ChREBP Nutrient-Sensing Factors in Metabolic Disease

Affiliations
Review

The Function of MondoA and ChREBP Nutrient-Sensing Factors in Metabolic Disease

Byungyong Ahn. Int J Mol Sci..

Abstract

Obesity is a major global public health concern associated with an increased risk of many health problems, including type 2 diabetes, heart disease, stroke, and some types of cancer. Obesity is also a critical factor in the development of insulin resistance and type 2 diabetes. Insulin resistance is associated with metabolic inflexibility, which interferes with the body's ability to switch from free fatty acids to carbohydrate substrates, as well as with the ectopic accumulation of triglycerides in non-adipose tissue, such as that of skeletal muscle, the liver, heart, and pancreas. Recent studies have demonstrated that MondoA (MLX-interacting protein or MLXIP) and the carbohydrate response element-binding protein (ChREBP, also known as MLXIPL and MondoB) play crucial roles in the regulation of nutrient metabolism and energy homeostasis in the body. This review summarizes recent advances in elucidating the function of MondoA and ChREBP in insulin resistance and related pathological conditions. This review provides an overview of the mechanisms by which MondoA and ChREBP transcription factors regulate glucose and lipid metabolism in metabolically active organs. Understanding the underlying mechanism of MondoA and ChREBP in insulin resistance and obesity can foster the development of new therapeutic strategies for treating metabolic diseases.

Keywords: ChREBP; MondoA; diabetes; insulin resistance; metabolic diseases; obesity.

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Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Gene expression levels of MLXIP and MLXIPL in different tissues. The tissue expression pattern of (A) MLXIP (https://gtexportal.org/home/gene/MLXIP (accessed on 12 May 2023)) and (B) MLXIPL (https://gtexportal.org/home/gene/MLXIPL (accessed on 12 May 2023)) are derived from GTEx Portal and presented with metabolic organs.
Figure 2
Figure 2
Regulation of MondoA and ChREBP activity by nutrients and post−translational modification (PTM). (A) MondoA transcriptional activity is elevated by glucose−6−phosphate (G6P), fructose-2,6−bisphosphate, non-glucose hexoses (allose, 3−O−methylglucose, and glucosamine), cellular acidosis, adenine nucleotides, and adenine−containing molecules, and is inhibited by glutamine and SBI−477/993. (B) ChREBP transcriptional activity is increased by G6P, F2,6BP, and xylulose−5−phosphate (Xu5P), and is decreased by ketone bodies, polyunsaturated fatty acids (PUFAs). Nuclear translocation of ChREBP is inhibited by its phosphorylation, regulated by PKA or AMPK. Acetylation (Ac) and O−GluNAcylation (OC) activate ChREBP transcriptional activity.
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