Abstract
Pancreatic β cells dedicate much of their protein translation capacity to producing insulin to maintain glucose homeostasis. In response to increased secretory demand, β cells can compensate by increasing insulin production capability even in the face of protracted peripheral insulin resistance. The ability to amplify insulin secretion in response to hyperglycemia is a critical facet of β-cell function, and the exact mechanisms by which this occurs have been studied for decades.To adapt to the constant and fast-changing demands for insulin production, β cells use the unfolded protein response of the endoplasmic reticulum. Failure of these compensatory mechanisms contributes to both type 1 and 2 diabetes. Additionally, studies in which β cells are “rested” by reducing endogenous insulin demand have shown promise as a therapeutic strategy that could be applied more broadly. Here, we review recent findings in β cells pertaining to the metabolic amplifying pathway, the unfolded protein response, and potential advances in therapeutics based on β-cell rest.
Original language | English (US) |
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Article number | bqab173 |
Journal | Endocrinology |
Volume | 162 |
Issue number | 11 |
DOIs | |
State | Published - Nov 1 2021 |
Keywords
- beta cell rest
- endoplasmic reticulum stress
- insulin secretion
- pancreatic islet beta cell
- unfolded protein response
ASJC Scopus subject areas
- Endocrinology