scholarly journals Photo-Switchable Sulfonylureas Binding to ATP-Sensitive Potassium Channel Reveal the Mechanism of Light-Controlled Insulin Release

2021 ◽  
Author(s):  
Katarzyna Walczewska-Szewc ◽  
Wieslaw Nowak
Keyword(s):  
Potassium Channel ◽  
Insulin Release

scholarly journals Modulation of Pancreatic Islet Electrophysiology and Insulin Release by Potassium Channel Subunit Kvbeta2

2015 ◽  
Vol 108 (2) ◽  
pp. 278a
Author(s):  
Peter Kilfoil ◽  
Oleg A. Barski ◽  
Aruni Bhatnagar
Keyword(s):  
Potassium Channel ◽  
Insulin Release ◽  
Pancreatic Islet

Potassium Channels in Hypokalaemic Periodic Paralysis: A Key to the Pathogenesis?

1993 ◽  
Vol 85 (3) ◽  
pp. 319-325 ◽  
Author(s):  
T. P. Links ◽  
A. J. Smit ◽  
H. J. G. H. Oosterhuis ◽  
W. D. Reitsma
Keyword(s):  
Muscle Strength ◽  
Potassium Channels ◽  
Potassium Channel ◽  
Insulin Release ◽  
Periodic Paralysis ◽  
Potassium Channel Opener ◽  
Glucose Loading ◽  
Control Subjects ◽  
Channel Opener ◽  
Hypokalaemic Periodic Paralysis

1. A possible role for the ATP-sensitive potassium channels in the pathogenesis of hypokalaemic periodic paralysis was investigated. 2. We assessed insulin release and muscle strength after intravenous glucose loading with and without the potassium channel opener pinacidil and the potassium channel blocker glibenclamide in three patients with hypokalaemic periodic paralysis and in a pair of matched control subjects for each patient. 3. A significantly higher initial insulin response (1.5-30 min) was found in the patients with hypokalaemic periodic paralysis in comparison with the control subjects. During potassium channel blocking with glibenclamide the insulin release was more enhanced in patients than in control subjects. On the other hand, the potassium channel opener pinacidil impaired the insulin release in healthy control subjects but not in patients. The serum glucose levels showed no differences between patients and control subjects. In one of the patients with hypokalaemic periodic paralysis glucose loading resulted in a fall in muscle strength, which did not occur during the administration of pinacidil. 4. These findings suggest a disturbance in the ATP-sensitive potassium channel in patients with hypokalaemic periodic paralysis, which is not limited to pancreatic β cells, but may be also involved in the abnormal behaviour of skeletal muscle.

3-(Alkylamino)-4H-pyrido[4,3-e]1,2,4-thiadiazine 1,1-dioxides as powerful inhibitors of insulin release from rat pancreatic B-cells: a new class of potassium channel openers?

1993 ◽  
Vol 36 (21) ◽  
pp. 3211-3213 ◽  
Author(s):  
Bernard Pirotte ◽  
Pascal de Tullio ◽  
Philippe Lebrun ◽  
Marie Helene Antoine ◽  
Jeanine Fontaine ◽  
...  
Keyword(s):  
B Cells ◽  
Potassium Channel ◽  
Insulin Release ◽  
Potassium Channel Openers ◽  
New Class ◽  
Pancreatic B Cells

Normal Insulin Release during Sustained Hyperglycaemia in Hypokalaemic Periodic Paralysis: Role of the Potassium Channel Opener Pinacidil in Impaired Muscle Strength

1996 ◽  
Vol 91 (5) ◽  
pp. 583-589 ◽  
Author(s):  
J. J. M. Ligtenberg ◽  
T. W. Van Haeften ◽  
L. E. Van Der Kolk ◽  
A. J. Smit ◽  
W. J. Sluiter ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Muscle Strength ◽  
Potassium Channel ◽  
Insulin Release ◽  
Periodic Paralysis ◽  
Second Phase ◽  
Potassium Channel Opener ◽  
Control Subjects ◽  
Channel Opener ◽  
Hypokalaemic Periodic Paralysis

1. Hypokalaemic periodic paralysis is characterized by attacks of muscle weakness. Glucose, insulin and an abnormal regulation of ATP-sensitive potassium channels may be involved in these attacks. We studied the effect of hyperglycaemia and of the potassium channel opener pinacidil on insulin release and muscle strength in patients with hypokalaemic periodic paralysis. 2. Insulin release was assessed on two occasions in four patients with hypokalaemic periodic paralysis and in eight matched control subjects, with and without treatment with 25 mg pinacidil orally, during a hyperglycaemic glucose clamp at a blood glucose level of 10 mmol/l, in a placebo-controlled, double-blind study. Muscle strength was measured in the hypokalaemic periodic paralysis patients before and during hyperglycaemia using a handheld dynamometer. 3. During the clamp, the mean glucose concentration (10–180 min) in control subjects was 9.9 ± 0.07 and 10.0 ± 0.03 mmol/l with and without pinacidil respectively, and in patients with hypokalaemic periodic paralysis was 10.0 ± 0.04 and 10.1 ± 0.06 mmol/l respectively (not significantly different). In both groups, the areas under the insulin curve from 0 to 10 min (first-phase insulin release) and from 30 to 180 min (second phase) were not different on the pinacidil study day compared with on the placebo day. The areas under the insulin curve of the first and second phases also did not differ between control subjects and patients with hypokalaemic periodic paralysis (with or without pinacidil). The M/I ratio, a measure of insulin sensitivity, was not different in the two groups. On the placebo day, baseline muscle strength in patients with hypokalaemic periodic paralysis was 165 ± 16 N for the hip abductors and 168 ± 19 N for the knee flexors. During the period of hyperglycaemia on the placebo day, muscle strength did not decrease in either muscle group. On the pinacidil study day, an increase in muscle strength was found only in the two hypokalaemic periodic paralysis patients with the lowest mean muscle strength (<150 N) on the placebo day. The two hypokalaemic periodic paralysis patients with a mean muscle strength on the placebo day >150N showed no increase in muscle strength with pinacidil. 4. Insulin secretion and sensitivity were normal in patients with hypokalaemic periodic paralysis. Hyperglycaemia during hyperglycaemic clamping did not provoke paralytic attacks and did not result in a decrease in muscle strength. The potassium channel opener pinacidil had no effect on insulin secretion in hypokalaemic periodic paralysis patients or in normal subjects. Pinacidil may enhance muscle strength in those hypokalaemic periodic paralysis patients who suffer partial paralytic attacks.

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