par Kalwat, Michael M.A.;Scheuner, Donalyn;Rodrigues-Dos-Santos, Karina;Eizirik, Decio L. 
;Cobb, Melanie M.H.
Référence Endocrinology, 162, 11
Publication Publié, 2021-11-01
;Cobb, Melanie M.H.Référence Endocrinology, 162, 11
Publication Publié, 2021-11-01
Article révisé par les pairs
| Résumé : | 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. |
