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Phosphate depletion reduces potassium-induced insulin secretion
G Z Fadda1, P Thanakitcharu, S G Massry
1Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.
Summary
Elevated resting calcium in pancreatic islets impairs potassium-induced insulin secretion. This occurs because high basal calcium reduces the calcium signal and its ratio to basal levels, hindering insulin release in phosphate-depleted rats.
Area of Science:
- Endocrinology
- Cell Physiology
- Renal Physiology
Background:
- Potassium-induced insulin secretion is crucial for glucose homeostasis.
- Chronic renal failure and phosphate depletion (PD) are associated with elevated basal cytosolic calcium ([Ca2+]i) in pancreatic islets.
- This elevated [Ca2+]i may impair insulin secretion by affecting calcium signaling.
Purpose of the Study:
- To investigate the impact of elevated basal [Ca2+]i on potassium-induced insulin secretion and calcium signaling in pancreatic islets.
- To determine if high basal [Ca2+]i interferes with the calcium signal magnitude and the delta [Ca2+]i/basal [Ca2+]i ratio.
Main Methods:
- Studied potassium-induced insulin secretion and calcium signaling in islets from phosphate-depleted (PD) rats and pair-weighed (PW) controls.
- Utilized verapamil to prevent elevated [Ca2+]i in PD and PW rats.
- Measured basal [Ca2+]i, calcium signal (delta [Ca2+]i), and the ratio delta [Ca2+]i/basal [Ca2+]i.
Main Results:
- PD rats exhibited significantly higher basal [Ca2+]i compared to PW rats.
- Insulin secretion, calcium signal, and delta [Ca2+]i/basal [Ca2+]i were significantly reduced in PD rats.
- Verapamil treatment normalized basal [Ca2+]i and restored these parameters in both PD and PW rats.
Conclusions:
- Elevated resting [Ca2+]i in pancreatic islets significantly impairs potassium-induced insulin secretion.
- High basal [Ca2+]i interferes with the calcium signal magnitude and the delta [Ca2+]i/basal [Ca2+]i ratio.
- These calcium-related derangements are a key factor in impaired insulin secretion in PD models.