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Published on: July 3, 2013
Impaired potassium-induced insulin secretion in chronic renal failure
G Z Fadda1, P Thanakitcharu, R Comunale
1Department of Medicine, University of Southern California School of Medicine, Los Angeles.
Kidney International
|September 1, 1991
Summary
Chronic renal failure (CRF) impairs potassium disposal due to excess parathyroid hormone (PTH). This study shows CRF impairs potassium-stimulated insulin secretion and calcium signaling in pancreatic islets, suggesting a mechanism for hyperkalemia in kidney disease.
Area of Science:
- Nephrology
- Endocrinology
- Physiology
Background:
- Extrarenal potassium disposal is impaired in chronic renal failure (CRF).
- This impairment is linked to excess parathyroid hormone (PTH) in CRF.
- Insulin aids potassium entry into cells, and hyperkalemia stimulates insulin secretion.
Purpose of the Study:
- To investigate if potassium-stimulated insulin secretion is impaired in CRF due to excess PTH.
- To examine the role of cytosolic calcium ([Ca2+]i) in this impaired secretion.
- To assess the impact of verapamil on these functions in normal and CRF rats.
Main Methods:
- Isolating pancreatic islets from normal, CRF, and CRF-PTX rats.
- Measuring potassium-stimulated insulin secretion and cytosolic calcium ([Ca2+]i) levels.
- Administering verapamil to normal and CRF rats to evaluate its effects.
Main Results:
- Potassium-stimulated insulin secretion was significantly lower in CRF rats compared to normal, CRF-PTX, and verapamil-treated groups.
- Basal cytosolic calcium ([Ca2+]i) levels were significantly higher in CRF rat islets.
- The calcium signal and ratio in response to potassium were significantly lower in CRF rat islets.
Conclusions:
- Excess PTH in chronic renal failure (CRF) impairs potassium-stimulated insulin secretion.
- This impairment is associated with altered cytosolic calcium ([Ca2+]i) handling in pancreatic islets.
- These defects contribute to abnormal extrarenal potassium disposal in CRF.
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