PXD006330

PXD006330 is an original dataset announced via ProteomeXchange.

Title	Adrenergic Receptor Stimulation Suppresses Metabolism in the Pancreatic β Cell
Description	Glucose-stimulated insulin secretion (GSIS) is suppressed through α-adrenergic receptor stimulation by catecholamines, epinephrine and norepinephrine, in pancreatic β-cells. Previous work has elucidated a bevy of adrenergic regulatory mechanisms beyond traditional Gi-coupled signaling including regulation of ion channels and interactions with exocytotic machinery. Glucose oxidation may also be an important site for adrenergic regulation of GSIS, but the link between epinephrine and glucose oxidation in β-cells is undefined. Here, we evaluate whether adrenergic stimulation decreases oxidative metabolism in β cells. Oxygen consumption rates were determined for Min6 and isolated rat islets in 20mM glucose complete media, then epinephrine was added at either 0 nM (vehicle control) or 100nM, followed by 10uM yohimbine (a selective Adrα2A antagonist). To identify glucose oxidation as the primary metabolic pathway affected by epinephrine, oxidation of 14C(U)-labeled glucose was determined in Min6 cells with epinephrine or vehicle. Oxygen consumption and glucose oxidation experiments were conducted in the presence of cAMP and insulin secretion blockers, respectively. Proteomics was performed on Min6 cells exposed to epinephrine for 4 hours and compared to controls. Epinephrine, but not vehicle, reduced (P<0.01) oxygen consumption rates in rat islets and Min6 cells to 64 ± 6% and 65 ± 1% of baseline, respectively, and yohimbine restored oxygen consumption to rates not different from baseline. In Min6 cells incubated with epinephrine rates of 14C glucose oxidation were reduced (P<0.01) 66 ± 4% compared to vehicle controls. These results demonstrate that acute epinephrine exposure suppresses glucose oxidation in β cells via the specific adrenergic receptor, Adrα2A, and indicate a new role for adrenergic regulation in GSIS.
HostingRepository	PRIDE
AnnounceDate	2019-11-08
AnnouncementXML	Submission_2019-11-08_08:10:04.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Ken Pendarvis
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	monohydroxylated residue; deamidated residue; iodoacetamide derivatized residue
Instrument	Velos Plus

Revision	Datetime	Status	ChangeLog Entry
0	2017-04-19 02:00:26	ID requested
⏵ 1	2019-11-08 08:10:05	announced

Kelly AC, Camacho LE, Pendarvis K, Davenport HM, Steffens NR, Smith KE, Weber CS, Lynch RM, Papas KK, Limesand SW, Adrenergic receptor stimulation suppresses oxidative metabolism in isolated rat islets and Min6 cells. Mol Cell Endocrinol, 473():136-145(2018) [pubmed]

curator keyword: Biological, Biomedical

submitter keyword: mouse, Min6, insulin, β-cells, pancreas, catecholamines, epinephrine, norepinephrine

Sean Limesand
contact affiliation	School of Comparative Animal and Biomedical Sciences University of Arizona Tucson, AZ USA
contact email	limesand@ag.arizona.edu
lab head
Ken Pendarvis
contact affiliation	Veterinary Science and Microbiology
contact email	jkpendarvis@email.arizona.edu
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD006330
     1. Label: PRIDE project
     2. Name: Adrenergic Receptor Stimulation Suppresses Metabolism in the Pancreatic β Cell