Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

Aims/hypothesis: The stress-activated nuclear protein transcription regulator 1 (NUPR1) is induced in response to glucose and TNF-α, both of which are elevated in type 2 diabetes, and Nupr1 has been implicated in cell proliferation and apoptosis cascades. We used Nupr1(-/-) mice to study the role of Nupr1 in glucose homeostasis under normal conditions and following maintenance on a high-fat diet (HFD).

Methods: Glucose homeostasis in vivo was determined by measuring glucose tolerance, insulin sensitivity and insulin secretion.