α₂-Adrenergic Disruption of β Cell BDNF-TrkB Receptor Tyrosine Kinase Signaling.

ABSTRACT: Adrenergic signaling is a well-known input into pancreatic islet function. Specifically, the insulin-secreting islet β cell expresses the G_i/o-linked α₂-adrenergic receptor, which upon activation suppresses insulin secretion. The use of the adrenergic agonist epinephrine at micromolar doses may have supraphysiological effects. We found that pretreating β cells with micromolar concentrations of epinephrine differentially inhibited activation of receptor tyrosine kinases. We chose TrkB as an example because of its relative sensitivity to the effects of epinephrine and due to its potential regulatory role in the β cell. Our characterization of brain-derived neurotrophic factor (BDNF)-TrkB signaling in MIN6 β cells showed that TrkB is activated by BDNF as expected, leadin

SUBMITTER: Kalwat MA 

PROVIDER: S-EPMC7593622 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature