However, SFRP4 does not control glucose homeostasis and β-cell mass in mice.

The islet β-cell is unusual in that glucose lacks an extracellular receptor.

This effect was not associated with enhanced β-cell proliferation or mass.

Type 2 diabetes incidence increases with age, while β-cell replication declines.

This was paralleled by an increase in β-cell proliferation and mass.

Insulin sensitivity and β-cell function were examined by homeostasis model assessment.

Of these, 16 had not previously been implicated in the regulation of β-cell mass.

Monogenic diabetes is caused by mutations that reduce β-cell function.

CAG repeat length did not show any significant correlation with IR or β-cell function.

In this study, we show how this coupling can produce oscillations in β-cell activity.

Here we show that palmitate-induced β-cell apoptosis is mediated by the intrinsic mitochondrial pathway.

Thus, MKP-1 is a possible target for anti-inflammatory therapeutic intervention with preservation of β-cell function.

Hence, factors controlling functional β-cell compensation are potentially important targets for the treatment of T2D.

Glycemia and β-cell function were assessed 1 week later at the peak of viral expression.

These data indicate that short-term HFD feeding enhances β-cell proliferation before insulin resistance becomes apparent.

Ex-4 nearly normalized both human β-cell survival and rodent β-cell replication when co-administered with tacrolimus.