CTRP4 ameliorates dexamethasoneinduced insulin resistance through the IRS1/PI3K/AKT pathway in 3T3L1 adipocytes

Maireyanmu Rouzi1, Xi Sun1, Luguang Sheng1

  • 1Department of Endocrinology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.

PubMed

Insights

Serum CTRP4 levels are negatively associated with insulin resistance (IR) in overweight and obese individuals. CTRP4 treatment in adipocytes reduced lipid accumulation and improved glucose uptake via the IRS-1/PI3K/AKT pathway.

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Molecular Biology

Background:

  • Obesity affects over 2.5 billion adults globally, contributing to insulin resistance (IR).
  • Adipose tissue dysfunction is a primary driver of IR pathogenesis in obesity.
  • C1q/TNF-related protein 4 (CTRP4) role in metabolic health requires further elucidation.

Purpose of the Study:

  • To investigate the association between serum CTRP4 levels and IR in overweight/obese patients.
  • To evaluate the effects and mechanisms of CTRP4 on IR in a cellular model.

Main Methods:

  • Serum CTRP4 levels measured by ELISA in 98 overweight/obese patients.
  • Correlation analysis between CTRP4 and HOMA-IR (homeostatic model assessment of IR).
  • In vitro study using dexamethasone-induced 3T3-L1 adipocytes to assess CTRP4 effects on lipid accumulation, glucose uptake, and insulin signaling pathway markers (IRS-1, PI3K, AKT, GLUT4) via western blotting.

Main Results:

  • Serum CTRP4 levels showed a negative correlation with BMI, HOMA-IR, waist, and abdomen circumference.
  • CTRP4 treatment significantly reduced lipid accumulation and increased glucose uptake in 3T3-L1 adipocytes.
  • CTRP4 elevated IRS-1, PI3K and AKT phosphorylation, and GLUT4 expression in IR adipocytes.

Conclusions:

  • Serum CTRP4 concentration is negatively correlated with insulin resistance in overweight/obese individuals.
  • CTRP4 demonstrates potential therapeutic effects by suppressing lipid accumulation and promoting glucose uptake.
  • CTRP4 exerts its effects through the IRS-1/PI3K/AKT signaling pathway, enhancing GLUT4 expression in adipocytes.

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