Glucocorticoids Reprogram β-Cell Signaling to Preserve Insulin Secretion.

ABSTRACT: Excessive glucocorticoid exposure has been shown to be deleterious for pancreatic β-cell function and insulin release. However, glucocorticoids at physiological levels are essential for many homeostatic processes, including glycemic control. We show that corticosterone and cortisol and their less active precursors 11-dehydrocorticosterone (11-DHC) and cortisone suppress voltage-dependent Ca²⁺ channel function and Ca²⁺ fluxes in rodent as well as in human β-cells. However, insulin secretion, maximal ATP/ADP responses to glucose, and β-cell identity were all unaffected. Further examination revealed the upregulation of parallel amplifying cAMP signals and an increase in the number of membrane-docked insulin secretory granules. Effects of 11-DHC could be prevented by lipo

SUBMITTER: Fine NHF 

PROVIDER: S-EPMC5780059 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature