FATP1 silence inhibits the differentiation and induces the apoptosis in chicken preadipocytes

Renli Qi1, Min Feng, Xiao Tan

  • 1College of Animal Science & Technology, Northwest A&F University, Yangling 712100, China.

Molecular Biology Reports
|November 29, 2012
PubMed

Insights

Fatty acid transport protein 1 (FATP1) deficiency in chicken preadipocytes inhibits differentiation and promotes apoptosis. Silencing FATP1 altered fatty acid transporter expression and key adipogenic factors, leading to reduced fat cell formation and increased cell death.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • Fatty acid transport protein 1 (FATP1) is crucial for free fatty acid trafficking in adipocytes.
  • The exact role of FATP1 and its interaction with other fatty acid transporters are not fully understood.

Purpose of the Study:

  • To investigate the function of FATP1 in chicken preadipocytes.
  • To elucidate the effects of FATP1 gene silencing on adipogenesis and apoptosis.

Main Methods:

  • FATP1 gene silencing was achieved using small interfering RNA (siRNA) in chicken preadipocytes.
  • Gene expression levels of fatty acid binding protein (FABP), fatty acid translocase (FAT), peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and fatty acid synthase (FAS) were analyzed.
  • Cell differentiation and apoptosis were assessed, including the activity of Caspase 3 and BCL2 associated X protein (Bax).

Main Results:

  • FATP1 silencing led to down-regulated FABP expression and up-regulated FAT expression.
  • Expressions of PPARγ, C/EBPα, and FAS were down-regulated, inhibiting adipogenesis.
  • FATP1 deficiency significantly increased the expression and activity of apoptotic factors Caspase 3 and Bax.
  • Cell differentiation was prevented, and apoptosis was induced in chicken preadipocytes.

Conclusions:

  • FATP1 plays a critical role in chicken preadipocyte differentiation.
  • FATP1 deficiency promotes apoptosis and inhibits adipogenesis by modulating key gene expressions and signaling pathways.

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