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Insulin release from isolated human fetal pancreatic islets
Science (New York, N.Y.)
|May 29, 1970
Summary
Human fetal islets (12-16 weeks gestation) showed early glucagon responsiveness. Insulin secretion was not significantly increased by glucose or tolbutamide in these developing pancreatic islets.
Area of Science:
- Endocrinology
- Developmental Biology
- Pancreatic Islet Research
Background:
- The development of pancreatic islet function is crucial for glucose homeostasis.
- Understanding the maturation of insulin and glucagon secretion in fetal development is essential.
Purpose of the Study:
- To investigate the responsiveness of isolated human fetal islets of Langerhans to various stimuli.
- To determine the gestational age at which human fetal islets acquire sensitivity to glucose, tolbutamide, and glucagon.
Main Methods:
- Human fetal pancreases (12-16 weeks gestation) were utilized.
- Islets of Langerhans were isolated using collagenase digestion.
- Isolated islets were incubated with buffer, glucose, tolbutamide, or glucagon, and insulin release was measured via immunoassay.
Main Results:
- Glucagon significantly increased insulin release from fetal islets above baseline levels.
- Glucose and tolbutamide did not significantly enhance insulin secretion in these fetal islets.
- These findings indicate differential maturation of stimulus-response pathways in developing human islets.
Conclusions:
- Human fetal islets at 12-16 weeks gestation demonstrate an early responsiveness to glucagon.
- Sensitivity to glucose and tolbutamide appears to develop later in gestation.
- This suggests a specific developmental timeline for nutrient-stimulated insulin secretion in the human pancreas.