The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity

Front Endocrinol (Lausanne). 2021 Mar 31:12:653972. doi: 10.3389/fendo.2021.653972. eCollection 2021.

Abstract

In the past several decades obesity has become one of the greatest health burdens worldwide. Diet high in fats and fructose is one of the main causes for the prevalence of metabolic disorders including obesity. Promoting brown or beige adipocyte development and activity is regarded as a potential treatment of obesity. Mondo family transcription factors including MondoA and carbohydrate response element binding protein (ChREBP) are critical for nutrient-sensing in multiple metabolic organs including the skeletal muscle, liver, adipose tissue and pancreas. Under normal nutrient conditions, MondoA and ChREBP contribute to maintaining metabolic homeostasis. When nutrient is overloaded, Mondo family transcription factors directly regulate glucose and lipid metabolism in brown and beige adipocytes or modulate the crosstalk between metabolic organs. In this review, we aim to provide an overview of recent advances in the understanding of MondoA and ChREBP in sensing nutrients and regulating obesity or related pathological conditions.

Keywords: ChREBP; MondoA; brown and beige adipose tissue; nutrient-sensing; obesity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipocytes / cytology
  • Adipocytes, Beige / metabolism*
  • Adipocytes, Brown / metabolism*
  • Adipogenesis
  • Adipose Tissue / metabolism
  • Animals
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / metabolism*
  • Energy Metabolism
  • Glucose / metabolism
  • Humans
  • Insulin / metabolism
  • Lipid Metabolism
  • Mice
  • Obesity / physiopathology
  • Obesity / therapy
  • Phenotype
  • Transcription Factors / metabolism*

Substances

  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • Insulin
  • MLXIP protein, human
  • MLXIPL protein, human
  • Mlxipl protein, mouse
  • MondoA protein, mouse
  • Transcription Factors
  • Glucose