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Insulin secretion in maturity-onset-diabetes. Function of isolated islets
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|August 1, 1980
Summary
Maturity onset diabetes (MOD) shows impaired insulin response. However, isolated beta-cells from MOD patients exhibit normal insulin levels and release, suggesting extrapancreatic factors, not intrinsic beta-cell defects, cause glucose response issues in MOD.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Diabetes Research
Background:
- Impaired insulin response to glucose is a hallmark of maturity onset diabetes (MOD).
- The underlying cause of this diminished response requires further investigation.
Purpose of the Study:
- To determine if the reduced in vivo insulin response in MOD is due to a primary defect in pancreatic beta-cells.
- To investigate insulin content, biosynthesis, and release from isolated MOD beta-cells.
Main Methods:
- Intraoperative biopsy of pancreatic islets from MOD patients.
- In vitro analysis of insulin content, biosynthesis, and glucose-stimulated insulin release from isolated islets.
Main Results:
- Isolated beta-cells from MOD patients demonstrated normal insulin content.
- Biosynthesis of insulin was normal or elevated, and glucose successfully stimulated insulin release in vitro.
- Despite in vitro responsiveness, in vivo insulin response remained impaired.
Conclusions:
- The primary defect in maturity onset diabetes is not an intrinsic failure of beta-cells to respond to glucose.
- Extrapancreatic factors likely play a significant role in modulating beta-cell function in MOD.
- These extrapancreatic factors may be elevated or exert a stronger inhibitory effect in diabetic patients.