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, therapeutic target, insulin resistance, adipogenesis, inflammation, type 2 diabetes.