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Insulin downregulates the expression of the Ca2+-activated nonselective cation channel TRPM5 in pancreatic islets

Barbara Colsoul1, Griet Jacobs, Koenraad Philippaert

  • 1Laboratory of Ion Channel Research, KU Leuven, Herestraat 49, bus 802, Leuven, 3000, Belgium.

Pflugers Archiv : European Journal of Physiology
|November 14, 2013
PubMed

Insights

Transient Receptor Potential Melastatin 5 (TRPM5) channel expression is reduced in type 2 diabetes models. Increased insulin levels downregulate TRPM5, impacting glucose homeostasis and insulin release.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Physiology

Background:

  • Transient Receptor Potential Melastatin 5 (TRPM5) cation channel is crucial for glucose-induced insulin release and homeostasis.
  • Dysregulation of TRPM5 may contribute to the pathophysiology of type 2 diabetes.

Purpose of the Study:

  • To investigate the expression and function of Trpm5 in pancreatic islets of mouse models for type 2 diabetes.
  • To explore the relationship between leptin, insulin, and Trpm5 expression in diabetes.

Main Methods:

  • Gene expression analysis of Trpm5 mRNA in pancreatic islets.
  • Assessment of glucose-induced Ca(2+) oscillations in islets.
  • Leptin treatment in ob/ob mice and insulin treatment in MIN6 cells.

Main Results:

  • Trpm5 mRNA levels were significantly reduced in db/db and ob/ob mice.
  • Glucose-induced Ca(2+) oscillations in db/db and ob/ob islets resembled Trpm5 (-/-) islets.
  • Leptin treatment upregulated Trpm5 in ob/ob mice, but insulin downregulated TRPM5 in MIN6 cells.

Conclusions:

  • Reduced Trpm5 expression is associated with type 2 diabetes in mice.
  • Elevated plasma insulin levels downregulate TRPM5 expression in pancreatic islets.
  • TRPM5 plays a role in the altered islet function observed in type 2 diabetes.

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