scholarly journals The Paradoxical Increase in Cortisol Secretion Induced by Dexamethasone in Primary Pigmented Nodular Adrenocortical Disease Involves a Glucocorticoid Receptor-Mediated Effect of Dexamethasone on Protein Kinase A Catalytic Subunits

2009 ◽  
Vol 23 (6) ◽  
pp. 945-945
Author(s):  
Estelle Louiset ◽  
Constantine A. Stratakis ◽  
Véronique Perraudin ◽  
Kurt J. Griffin ◽  
Rossella Libé ◽  
...  
1992 ◽  
Vol 6 (9) ◽  
pp. 1451-1457 ◽  
Author(s):  
P N Rangarajan ◽  
K Umesono ◽  
R M Evans

2005 ◽  
Vol 73 (9) ◽  
pp. 591-596 ◽  
Author(s):  
Huiping Zhu ◽  
Wei Lu ◽  
Cecile Laurent ◽  
Gary M. Shaw ◽  
Edward J. Lammer ◽  
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2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Karim Salhadar ◽  
V. Raghuram ◽  
Chin-Rang Yang ◽  
Kavee Limbutara ◽  
Mark Knepper

2002 ◽  
Vol 368 (2) ◽  
pp. 397-404 ◽  
Author(s):  
Zhiyong GAO ◽  
Robert A. YOUNG ◽  
Matteo M. TRUCCO ◽  
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...  

Activation of protein kinase A (cAMP-dependent protein kinase; PKA) triggers insulin secretion in the β-cell. Adenylate cyclase toxin (ACT), a bacterial exotoxin with adenylate cyclase activity, and forskolin, an activator of adenylate cyclase, both dose-dependently increased insulin secretion in the presence, but not the absence, of glucose in insulin-secreting βTC3 cells. The stimulation of cAMP release by either agent was dose-dependent but glucose-independent. Omission of extracellular Ca2+ totally abolished the effects of ACT on insulin secretion and cytosolic cAMP accumulation. ACT and forskolin caused rapid and dramatic increases in cytosolic Ca2+, which were blocked by nifedipine and the omission of extracellular Ca2+. Omission of glucose completely blocked the effects of forskolin and partially blocked the effects of ACT on cytosolic Ca2+. PKA α, β and γ catalytic subunits (Cα, Cβ and Cγ respectively) were identified in βTC6 cells by confocal microscopy. Glucose and glucagon-like polypeptide-1 (GLP-1) caused translocation of Cα to the nucleus and of Cβ to the plasma membrane and the nucleus, but did not affect the distribution of Cγ. In conclusion, glucose and GLP-1 amplify insulin secretion via cAMP production and PKAβ activation.


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