IP3R1 mutation perturbs glucose homeostasis

Ye and colleagues created a line of transgenic mice in which they serendipitously observed that males exhibited elevated fasting blood glucose associated with a decrease in blood insulin which then developed progressive glucose intolerance. They found that the IP3R 1-encoding gene (Itpr1) in these D2D mice had been disrupted. IP3Rs are ligand-gated Ca2+ channels which modulate cellular processes.

Ye and colleagues used the opt/+ mouse model (an alternative to their D2D line) to examine the role of IP3R1 in glucose metabolism, finding that, at the age of 10 weeks, the male mice developed glucose intolerance whilst on a regular diet and showed a decrease in glucose-stimulated blood insulin level, reduced beta cell mass and insulin content. Fed a high-fat diet, opt/+ mice were more susceptible to the development of hyperglycemia, glucose intolerance and insulin resistance, suggesting a predisposition to diabetes. Ye et al. (2011) Journal of Endocrinology 210 209-217.

Read the full article at: DOI:10.1530/JOE-11-0012.