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Lactation-induced changes in calcium handling by rat pancreatic islets
Journal of Developmental Physiology
|February 1, 1987
Summary
Lactation impairs glucose-stimulated insulin release by altering calcium handling in pancreatic islets. This suggests a depletion of calcium stores contributes to reduced insulin secretion during lactation.
Area of Science:
- Endocrinology
- Cell Biology
- Metabolic Research
Background:
- Lactation is associated with altered glucose metabolism.
- Pancreatic islets regulate insulin secretion in response to glucose.
- Calcium ions play a critical role in insulin release.
Purpose of the Study:
- To investigate the mechanisms underlying impaired glucose-stimulated insulin release in lactating rats.
- To examine the role of calcium handling in lactation-induced insulin secretion defects.
Main Methods:
- Isolated pancreatic islets from lactating and non-lactating rats were used.
- Insulin release was measured under various conditions, including stimulation with glucose, gliclazide, and calcium agonists.
- 45Ca outflow and sequestration were assessed using radiolabeling techniques.
- Calcium-ionophoretic effects of islet extracts were evaluated.
Main Results:
- Insulin release in response to glucose was reduced in islets from lactating rats.
- Gliclazide and calcium agonists restored glucose-stimulated insulin release.
- Lactation favored 45Ca sequestration into non-labile pools within islets stimulated by gliclazide.
- Islet extracts from lactating rats exhibited a higher calcium-ionophoretic effect.
Conclusions:
- Reduced insulin secretory responsiveness to D-glucose during lactation is partly due to a depletion of endogenous calcium stores.
- Lactation appears to enhance cellular systems involved in calcium entry and sequestration within islet cells.
- These alterations in calcium dynamics contribute to the observed defect in insulin secretion.