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Resistin induces rat insulinoma cell RINm5F apoptosis

Chun-lin Gao1, De-yu Zhao, Jie Qiu

  • 1Department of Pediatrics, Nanjing Maternity & Child Health Hospital of Nanjing Medical University, Nanjing, China.

Molecular Biology Reports
|October 8, 2008
PubMed

Insights

Resistin, a protein linked to obesity and type 2 diabetes, causes beta-cell apoptosis. Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) prevents this resistin-induced beta-cell death.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Diabetes Research

Background:

  • Adipokines, such as resistin, are implicated in beta-cell dysfunction and apoptosis in type 2 diabetes.
  • Resistin is associated with obesity and type 2 diabetes, and it impairs glucose-stimulated insulin secretion (GSIS) in beta-cells.

Purpose of the Study:

  • To investigate the effects of resistin on rat insulinoma cells (RINm5F).
  • To determine the protective role of Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) against resistin-induced beta-cell damage.

Main Methods:

  • Treatment of RINm5F cells with resistin and TIMP-1.
  • Assay of caspase-3 activity and DNA fragmentation to assess apoptosis.
  • Analysis of Akt and IkB-alpha phosphorylation to elucidate molecular mechanisms.

Main Results:

  • Resistin treatment induced cell damage, caspase-3 activation, and DNA ladder formation in RINm5F cells.
  • TIMP-1 significantly protected against resistin-mediated cytotoxicity.
  • TIMP-1 attenuated resistin's effects by modulating Akt and IkB-alpha phosphorylation pathways.

Conclusions:

  • Resistin induces beta-cell apoptosis through mechanisms involving caspase-3 activation and DNA damage.
  • TIMP-1 effectively prevents resistin-induced beta-cell apoptosis.
  • The protective effect of TIMP-1 involves the modulation of Akt and IkB-alpha signaling pathways.

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