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Glucose metabolism in mouse pancreatic islets
The Biochemical Journal
|June 1, 1970
Summary
Glucose metabolism in mouse islets is sensitive to glucose concentration, with mannoheptulose and glucosamine inhibiting glucose phosphorylation. These findings suggest glucose metabolism mediates glucose-stimulated insulin release.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Pancreatic islets are crucial for insulin secretion.
- Glucose metabolism plays a key role in regulating insulin release.
- Understanding glucose utilization pathways in islets is essential for diabetes research.
Purpose of the Study:
- To investigate glucose oxidation, lactate output, and glucose 6-phosphate levels in mouse pancreatic islets.
- To determine the effects of various substances on glucose metabolism and insulin release pathways.
- To elucidate the role of glucose phosphorylation in glucose-stimulated insulin secretion.
Main Methods:
- Measurement of glucose oxidation via (14)CO(2) formation from [U-(14)C]glucose.
- Assessment of lactate production and intracellular glucose 6-phosphate concentrations.
- In vitro incubation of mouse pancreatic islets with varying glucose concentrations and inhibitors.
Main Results:
- Glucose oxidation rate was highly dependent on extracellular glucose, particularly between 1-2 mg/ml.
- Mannose and fructose were oxidized but less efficiently than glucose, with poor interconversion.
- Inhibitors like mannoheptulose and glucosamine affected glucose phosphorylation and lactate output, while tolbutamide stimulated lactate production.
Conclusions:
- Glucose utilization in mouse islets may be limited by glucose phosphorylation rate.
- Mannose metabolism shows poor equilibration between fructose 6-phosphate and glucose 6-phosphate.
- Glucose metabolism, influenced by glucose phosphorylation, likely mediates glucose-stimulated insulin release.