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Rosiglitazone counteracts palmitate-induced beta-cell dysfunction by suppression of MAP kinase, inducible nitric

S Meidute Abaraviciene1, I Lundquist, A Salehi

  • 1Department of Clinical Science, Division of Endocrine Pharmacology, UMAS, CRC, 205 02, Malmö, Sweden.

Cellular and Molecular Life Sciences : CMLS
|June 19, 2008
PubMed

Insights

The anti-diabetic drug rosiglitazone (ROZ) protects pancreatic beta-cells from palmitate-induced dysfunction. ROZ counteracts harmful effects by reducing inflammation, pro-apoptotic signaling, and restoring insulin secretion.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Pharmacology

Background:

  • Chronic exposure to elevated palmitate levels impairs pancreatic beta-cell function.
  • Mitogen-activated protein kinases (MAPKs) and caspase-3 are implicated in palmitate-induced beta-cell dysfunction.

Purpose of the Study:

  • To investigate the role of MAPKs and caspase-3 in palmitate-induced beta-cell dysfunction.
  • To evaluate the protective effects of rosiglitazone (ROZ) against palmitate-induced damage.

Main Methods:

  • Incubation of pancreatic islets and MIN6c4-cells with palmitate and/or ROZ.
  • Measurement of intracellular calcium, insulin secretion, MAPK phosphorylation, inducible nitric oxide synthase (iNOS) expression, and caspase-3 activity.
  • Assessment of glucose-stimulated insulin release after treatment.

Main Results:

  • Palmitate amplified glucose-stimulated insulin secretion and calcium levels; ROZ suppressed this amplification.
  • ROZ inhibited palmitate-induced phosphorylation of SAPK/JNK and p38 MAPKs.
  • Long-term palmitate exposure increased iNOS and activated SAPK/JNK-p38, effects counteracted by ROZ.
  • Palmitate and cytokines activated caspase-3; ROZ suppressed palmitate-induced activation.
  • ROZ restored glucose-stimulated insulin release inhibited by palmitate exposure.

Conclusions:

  • Rosiglitazone (ROZ) protects pancreatic beta-cells from palmitate-induced dysfunction.
  • ROZ mitigates palmitate's adverse effects by suppressing iNOS, pro-apoptotic MAPKs, and caspase-3 activation.
  • ROZ effectively restores impaired glucose-stimulated insulin release in beta-cells exposed to palmitate.

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