scholarly journals PKA‐independent cAMP stimulation of white adipocyte exocytosis and adipokine secretion: modulations by Ca2+and ATP

2014 ◽  
Vol 592 (23) ◽  
pp. 5169-5186 ◽  
Author(s):  
Ali M. Komai ◽  
Cecilia Brännmark ◽  
Saliha Musovic ◽  
Charlotta S. Olofsson

1985 ◽  
Vol 100 (3) ◽  
pp. 715-720 ◽  
Author(s):  
C Klein ◽  
J Lubs-Haukeness ◽  
S Simons

Stimulation, within 1 min after cAMP stimulation, of aggregation-competent Dictyostelium discoideum amebae was found to cause a rapid (within 1 min) modification of the cell's surface cAMP receptor. The modified receptor migrated on SDS PAGE as a 47,000-mol-wt protein, as opposed to a 45,000-mol-wt protein labeled on unstimulated cells. The length of time this modified receptor could be detected depended upon the strength of the cAMP stimulus: 3-4 min after treatment with 10(-7) M cAMP, cells no longer possessed the 47,000-mol-wt form of the cAMP receptor. Instead, the 45,000-mol-wt form was present. Stimulation of cells with 10(-5) M cAMP, however, resulted in the persistent (over 15 min) expression of the modified receptor. The time course, concentration dependence, and specificity of stimulus for this cAMP-induced shift in the cAMP receptor were found to parallel the cAMP-stimulated phosphorylation of a 47,000-mol-wt protein. In addition, both phenomena were shown to occur in the absence of endogenous cAMP synthesis. The possibility that the cAMP receptor is phosphorylated in response to cAMP stimulation, and the role of this event in cell desensitization, are discussed.



Endocrinology ◽  
1973 ◽  
Vol 93 (6) ◽  
pp. 1287-1293 ◽  
Author(s):  
BERNARD A. ROOS


2000 ◽  
pp. 60-65 ◽  
Author(s):  
J Benicky ◽  
V Strbak

OBJECTIVE: Pancreatic TRH is present in insulin-producing B-cells of the islets of Langerhans. There is fragmentary evidence that it may be involved in glucoregulation. The aim of our present study was to analyze how glucose and insulin affect TRH secretion by the pancreatic islets. DESIGN: Isolated pancreatic islets were incubated with different concentrations of glucose, insulin and glucagon, and TRH release was measured. RESULTS: In the present study, 6 and 12mmol/l d-glucose caused significant TRH release from isolated adult rat pancreatic islets when compared with that in the presence of the same concentrations of biologically ineffective l-glucose. Thirtymmol/l d-glucose was also ineffective, but this was not due to depression of secretion by hyperosmolarity since isosmotic compensation for the high glucose addition did not restore its stimulatory effect. Five micromol/l dibutyryl cyclic 3',5'-adenosine monophosphate (db-cAMP) increased both basal and glucose-stimulated TRH release, but this effect was not seen with 50micromol/l db-cAMP. Stimulation of phosphodiesterase by imidazole resulted in decreased basal but not glucose-stimulated release of TRH. Glucagon (10(-7)mol/l) did not affect either basal or glucose-stimulated release of TRH, while insulin (10(-7) and 10(-6)mol/l) inhibited both. CONCLUSION: Our present data showing that glucose stimulates and insulin inhibits pancreatic TRH release are compatible with the possibility that this substance may play a role in glucoregulation.



1996 ◽  
Vol 432 (3) ◽  
pp. 516-522 ◽  
Author(s):  
M. Mall ◽  
K. Kunzelmann ◽  
A. Hipper ◽  
R. Greger ◽  
A. E. Busch


1987 ◽  
Vol 21 (4) ◽  
pp. 240A-240A
Author(s):  
Kenneth T Nakamura ◽  
Beth M Alden ◽  
Pedro A Jose ◽  
G Paul Matherne ◽  
Jean E Robillard


1997 ◽  
Vol 272 (33) ◽  
pp. 20736-20741 ◽  
Author(s):  
Maria Assunta Bevilacqua ◽  
Maria Concetta Faniello ◽  
Barbara Quaresima ◽  
Maria Teresa Tiano ◽  
Paola Giuliano ◽  
...  




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