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Magnesium uptake by pancreatic islet cells is modulated by stimulators and inhibitors of the B-cell function
Abstract:
28Mg2+ uptake by rat islets was measured during incubation with various stimulators or inhibitors of insulin release. D-Glucose induced a dose-dependent increase in 28Mg2+ uptake after 10 min or 120 min. The threshold concentration was around 6 mM and the maximum effect was observed with 15-20 mM glucose. After 120 min 28Mg2+ uptake was also stimulated by the metabolized sugars mannose, N-acetylglucosamine or glyceraldehyde, was unaffected by the non-metabolized or poorly metabolized L-glucose, galactose, 3-O-methylglucose, 2-deoxyglucose, fructose or mannoheptulose and was inhibited by glucosamine. The effect of glucose was markedly impaired by mannoheptulose, glucosamine, aminooxyacetate and NH4Cl, but was only partially decreased by D600 or diazoxide, which were ineffective in a glucose-free medium. Tolbutamide or KCl slightly increased 28Mg2+ uptake. Alanine, leucine alone or with glutamine, and ketoisocaproate also stimulated 28Mg2+ uptake, whereas arginine and lysine decreased it. These changes in 28Mg2+ uptake, brought about by various modifiers of the B-cell function, are thus similar but not identical to the changes in Ca2+ uptake, and are not the consequence of insulin release. The stimulatory effect of glucose requires glucose metabolism by islet cells, but is only partially due to depolarization of the B-cell membrane.
Insights
Magnesium-28 (28Mg2+) uptake in rat islets increases with glucose, requiring glucose metabolism. This uptake is influenced by various insulin secretagogues and inhibitors, showing distinct patterns from calcium (Ca2+) uptake.
Area of Science:
- Endocrinology
- Cell Physiology
- Metabolic Research
Background:
- Insulin secretion from pancreatic beta-cells is a complex process.
- Magnesium (Mg2+) plays a crucial role in cellular functions, including insulin release.
- Understanding Mg2+ dynamics in islets provides insights into metabolic regulation.
Purpose of the Study:
- To investigate the uptake of 28Mg2+ by rat islets under various conditions.
- To compare 28Mg2+ uptake patterns with those of Ca2+ uptake.
- To elucidate the relationship between glucose metabolism and Mg2+ transport in islet cells.
Main Methods:
- Incubation of isolated rat islets with 28Mg2+.
- Exposure to different concentrations of D-glucose and other sugars.
- Treatment with insulin secretagogues (e.g., tolbutamide, KCl, amino acids) and inhibitors (e.g., mannoheptulose, D600).
- Measurement of 28Mg2+ uptake over time.
Main Results:
- D-Glucose stimulated 28Mg2+ uptake in a dose-dependent manner, with a threshold around 6 mM.
- Metabolized sugars (mannose, N-acetylglucosamine, glyceraldehyde) stimulated uptake, while non-metabolized sugars did not.
- Glucose-induced uptake was impaired by inhibitors of glucose metabolism and partially affected by depolarization agents.
- Changes in 28Mg2+ uptake mirrored, but were not identical to, Ca2+ uptake changes and were independent of insulin release itself.
Conclusions:
- Glucose-induced 28Mg2+ uptake is dependent on glucose metabolism within islet cells.
- The observed Mg2+ uptake is not a direct consequence of insulin release.
- The findings suggest a distinct role for magnesium transport in beta-cell function beyond calcium dynamics.