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Adrenaline stimulates glucagon secretion by Tpc2-Dependent ca2+ mobilization from acidic stores in pancreatic a-Cells

Artikel i vetenskaplig tidskrift
Författare A. Hamilton
Q. Zhang
Albert Salehi
M. Willems
J. G. Knudsen
A. K. Ringgaard
C. E. Chapman
A. Gonzalez-Alvarez
N. C. Surdo
M. Zaccolo
D. Basco
P. R. V. Johnson
R. Ramracheya
G. A. Rutter
A. Galione
Patrik Rorsman
A. I. Tarasov
Publicerad i Diabetes
Volym 67
Nummer/häfte 6
Sidor 1128-1139
ISSN 0012-1797
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 1128-1139
Språk en
Länkar dx.doi.org/10.2337/db17-1102
Ämneskategorier Diabetologi

Sammanfattning

Adrenaline is a powerful stimulus of glucagon secretion. It acts by activation of b-adrenergic receptors, but the downstream mechanisms have only been partially elucidated. Here, we have examined the effects of adrenaline in mouse and human a-cells by a combination of electrophysiology, imaging of Ca2+ and PKA activity, and hormone release measurements. We found that stimulation of glucagon secretion correlated with a PKA- and EPAC2-dependent (inhibited by PKI and ESI-05, respectively) elevation of [Ca2+]i in a-cells, which occurred without stimulation of electrical activity and persisted in the absence of extracellular Ca2+ but was sensitive to ryanodine, bafilomycin, and thapsigargin. Adrenaline also increased [Ca2+]i in a-cells in human islets. Genetic or pharmacological inhibition of the Tpc2 channel (that mediates Ca2+ release from acidic intracellular stores) abolished the stimulatory effect of adrenaline on glucagon secretion and reduced the elevation of [Ca2+]i. Furthermore, in Tpc2-deficient islets, ryanodine exerted no additive inhibitory effect. These data suggest that b-adrenergic stimulation of glucagon secretion is controlled by a hierarchy of [Ca2+]i signaling in the a-cell that is initiated by cAMP-induced Tpc2-dependent Ca2+ release from the acidic stores and further amplified by Ca2+-induced Ca2+ release from the sarco/endoplasmic reticulum. © 2018 by the American Diabetes Association.

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