Elsewhere, collectrin is involved in pancreatic β cell proliferation and insulin secretion.

The oral minimal model was used to measure β cell function.

Pancreatic β cell area was significantly increased in the IT group.

These results uncover LIN28B as a modulator of β cell maturation in vitro.

We show here that the β cell population in situ is operationally heterogeneous.

Glucose-evoked mitochondrial signals augment ATP synthesis in the pancreatic β cell.

Immunotherapy can attenuate T cell responses against β cell antigens.

The engrafted β-like cells expressed β cell transcription factors and markers associated with functional maturity.

This improvement was associated with attenuated β cell senescence.

Despite markedly stimulating β cell proliferation during regeneration, NECA had only a modest effect during development.

Thus, β cell dysfunction results from enhanced insulin secretion combined with an arrest of insulin synthesis.

We have recently demonstrated that matrix pH increases during nutrient stimulation of the pancreatic β cell.

These findings reveal the role that altered Ca2+ sensing plays in regulating β cell maturation.

Although PERK excision increased β cell death, this was not a result of decreased proliferation as previously reported.

We identified that NF-kB-dependent induction of iNOSiNOS is a critical determinant of β cell fate following cytokine exposure.

Hubs were metabolically adapted and targeted by both pro-inflammatory and glucolipotoxic insults to induce widespread β cell dysfunction.