Maturation of the response of human fetal pancreatic explants to glucose
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Human fetal pancreas insulin release matures with age, showing a significant response by 55 weeks. This suggests potential for fetal pancreatic tissue in treating diabetes mellitus.
Area of Science:
- Endocrinology
- Developmental Biology
- Regenerative Medicine
Background:
- Insulin release in response to glucose is diminished in fetuses compared to infants and adults.
- Understanding the maturation of this glucose-stimulated insulin secretion (GSIS) is crucial for therapeutic applications.
Purpose of the Study:
- To systematically examine the maturation of glucose-stimulated insulin release from human fetal pancreatic tissue.
- To assess the potential of human fetal pancreatic tissue for diabetes mellitus treatment.
Main Methods:
- Human pancreases (14-20 weeks gestation) were cultured or passaged in diabetic nude mice.
- Tissue from 14 to 58 weeks gestation was stimulated with glucose in vitro.
- Implant viability and function were assessed in vivo.
Main Results:
- Glucose-stimulated insulin release was first observed at 25 weeks gestation.
- A dramatic increase in insulin response was noted in fetal tissue aged 55 weeks and older.
- A nude mouse model demonstrated normoglycemia with a 52-week-old pancreatic implant, which recurred upon removal.
Conclusions:
- Human fetal pancreatic insulin secretion matures significantly during gestation.
- These findings support the therapeutic potential of human fetal pancreatic tissue for treating diabetes mellitus.
Abstract:
The release of insulin from the human pancreas in response to glucose is known to be either poor or absent in the fetus, whereas in the infant and adult, the response is much greater. The maturation of this response was examined systematically in this study using pancreases that were initially obtained at 14-20 weeks gestation and maintained either in culture alone or by passaging them in diabetic nude mice. Stimulation with glucose was carried out in vitro using tissue of ages ranging from 14 to 58 weeks. A response to glucose was initially seen at 25 weeks and this dramatically increased in the fetal tissue that had reached an age of 55 weeks or more. One of the nude mice used for passage developed normoglycaemia and when the pancreatic implant of age 52 weeks was removed, diabetes recurred. Our findings support the idea of the use of human fetal pancreatic tissue in the treatment of diabetes mellitus.