GATA-3 as a Potential Therapeutic Target for Insulin Resistance and Type 2 Diabetes Mellitus

Curr Diabetes Rev. 2021;17(2):169-179. doi: 10.2174/1573399816666200705210417.

Abstract

Impaired adipogenesis plays an important role in the development of obesity-associated insulin resistance and type 2 diabetes as it leads to ectopic fat deposition. The anti-adipogenic transcription factor GATA-3 was identified as one of the potential molecular targets responsible for the impairment of adipogenesis. The expression of GATA-3 is higher in insulinresistant obese individuals compared to BMI-matched insulin-sensitive counterparts. Adipose tissue inflammation is a crucial mediator of this process. Hyperglycemia mediates the activation of the immune system, partially through upregulation of GATA- 3, causing exacerbation of the inflammatory state associated with obesity. This review discusses the evidence supporting the inhibition of GATA-3 as a useful therapeutic strategy in obesity-associated insulin resistance and type 2 diabetes, through up-regulation adipogenesis and amelioration of the immune response.

Keywords: GATA-3; adipogenesis; inflammation; insulin resistance; therapeutic target; type 2 diabetes.

Publication types

  • Review

MeSH terms

  • Adipogenesis
  • Adipose Tissue
  • Diabetes Mellitus, Type 2* / drug therapy
  • Humans
  • Inflammation / drug therapy
  • Insulin Resistance*
  • Obesity / complications
  • Obesity / drug therapy