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TAp63 is correlated with chronic inflammation in patients with newly diagnosed type 2 diabetes mellitus

Xuemei Hu1, Jie Liu1, Li Sun1

  • 1Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.

Journal of Diabetes and Its Complications
|February 4, 2018
PubMed
Abstract

Insights

TAp63 expression is lower in type 2 diabetes mellitus (T2DM) patients and correlates negatively with inflammation and metabolic dysfunction. Glucose and palmitic acid treatments increased TAp63 levels in cells.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Immunology

Background:

  • Type 2 Diabetes Mellitus (T2DM) is a complex metabolic disorder characterized by chronic inflammation and impaired glucose and lipid metabolism.
  • The role of TAp63, a p53 family member, in the pathogenesis of T2DM remains largely unexplored.

Purpose of the Study:

  • To investigate TAp63 expression in patients with T2DM.
  • To explore the correlation between TAp63 levels, proinflammatory cytokines, and clinical parameters in T2DM.
  • To examine the effect of high glucose and palmitic acid on TAp63 expression in vitro.

Main Methods:

  • Peripheral blood mononuclear cells (PBMCs) and plasma were collected from 72 T2DM patients and 72 healthy controls.
  • Clinical parameters, insulin resistance (HOMA-IR), and plasma levels of TNF-α and IL-6 were assessed.
  • TAp63 expression in PBMCs was analyzed via qRT-PCR and Western blot, and its response to glucose and palmitic acid in cultured PBMCs was evaluated.

Main Results:

  • TAp63 expression was significantly lower in T2DM patients compared to controls.
  • TAp63 expression negatively correlated with fasting blood glucose (FBG), fasting insulin (FIN), HbA1c, HOMA-IR, free fatty acids (FFAs), TNF-α, and IL-6.
  • In vitro, treatment with high glucose or palmitic acid increased TAp63 expression in PBMCs.

Conclusions:

  • TAp63 levels may be associated with the chronic inflammatory state observed in T2DM.
  • Perturbed glucose and lipid metabolism in T2DM might be linked to altered TAp63 expression.
  • TAp63 warrants further investigation as a potential biomarker or therapeutic target in T2DM.
Keywords:
InflammationInsulin resistanceNuclear factor-κBTAp63Type 2 diabetes mellitus

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