scholarly journals The Adenylate cyclase-cyclic AMP system in islets of langerhans and its role in the control of insulin release

Diabetologia ◽  
1979 ◽  
Vol 16 (5) ◽  
pp. 287-296 ◽  
Author(s):  
G. W. G. Sharp
1981 ◽  
Vol 96 (2) ◽  
pp. 222-226 ◽  
Author(s):  
Loren G. Lipson ◽  
Michael J. Bush ◽  
Gretchen E. Tietjen ◽  
Aeree Yoon

Abstract. In attempting to understand the causes of the hyperglycaemia observed in aging populations and to determine the mechanism(s) for the diminished in vitro insulin release from islets of Langerhans of older rats, the adenylate cyclase-cyclic AMP system was studied in isolated islets from 12 month old and 2½ month old (control) male rats to determine its role in this altered insulin secretion. Islets of Langerhans were isolated by collagenase digestion and then either incubated in the presence of low or high concentrations of glucose for studies of insulin release or were sonicated and assayed for determinations of activities of adenylate cyclase and phosphodiesterase. Insulin release was identical from islets of 12 month old and 2½ month old rats to 2.8 mm D-glucose, while in the presence of 16.7 mm D-glucose, insulin release was decreased by 33% (P < 0.02) from islets of the older animals. Adenylate cyclase activity was diminished by 60% (P < 0.005) from the 12 month old rats as compared with islets from the 2½ month old controls, while low Km phosphodiesterase activity was similar in islets from both groups of animals. From these studies it appears that the adenylate cyclase-cyclic AMP system may play a role in the altered insulin release from islets of aging rats.


1976 ◽  
Vol 81 (4) ◽  
pp. 743-752 ◽  
Author(s):  
S. Efendić ◽  
R. Luft ◽  
A. Claro

ABSTRACT Somatostatin in as small a dose as 70 μg given over a period of 90 min to seven healthy subjects inhibited insulin release induced by glucose (500 mg/kg as a bolus ± 20 mg/kg/min). This inhibition seemed to be of competitive nature since the effect was nearly overcome when the glucose dose was raised considerably. Somatostatin in nine subjects also inhibited insulin release induced by glucagon and tolbutamide, and this inhibition was of the same order of magnitude as that of glucose induced insulin release. Since all these insulinogogues enhance the accumulation of cyclic AMP in the β-cells, it is suggested that the adenylate cyclase-cyclic AMP system might be involved in the action of somatostatin. Somatostatin did not seem to interfere with the glycogenolytic effect of glucagon on the liver.


Diabetes ◽  
1980 ◽  
Vol 29 (1) ◽  
pp. 74-77 ◽  
Author(s):  
G. W. G. Sharp ◽  
D. E. Wiedenkeller ◽  
D. Kaelin ◽  
E. G. Siegel ◽  
C. B. Wollheim

1975 ◽  
Vol 53 (10) ◽  
pp. 1122-1127 ◽  
Author(s):  
J. A. C. Harrow ◽  
J. N. Singh ◽  
G. Jasmin ◽  
N. S. Dhalla

Cyclic AMP content, adenylate cyclase (EC 4.6.1.1) activity and phosphodiesterase I (EC 3.1.4.1) activity of the hind leg skeletal muscle and cardiac muscle in 60- and 150-day-old normal and myopathic (UM-X7.1) hamsters were examined. In 60-day-old myopathic animals, cardiac cyclic AMP levels were higher and phosphodiesterase I activity was lower, without any changes in the basal adenylate cyclase activity, whereas in 150-day-old myopathic hamsters, cardiac cyclic AMP and basal adenylate cyclase activity were lower, without any changes in the homogenate phosphodiesterase I activity. On the other hand, basal adenylate cyclase and phosphodiesterase I activities in the skeletal muscle homogenate from 60- and 150-day-old myopathic animals were not different from the normal values but the skeletal muscle cyclic AMP levels were significantly less in 60-day-old myopathic hamsters only. The plasma cyclic AMP levels in 60-day-old myopathic hamsters, unlike 150-day-old myopathic animals, were higher than the normal. Although these results reveal differences in myopathic cardiac and skeletal muscles, it is concluded that changes in adenylate cyclase – cyclic AMP system in myopathy are dependent upon the degree of disease.


Sign in / Sign up

Export Citation Format

Share Document