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Ectopic Expression of GIP in Pancreatic β-Cells Maintains Enhanced Insulin Secretion in Mice With Complete Absence of Proglucagon-Derived Peptides
Producing GIP in insulin-making cells keeps insulin release high in mice lacking certain gut hormones
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Abstract
Gcg-deficient mice exhibited improved glucose tolerance and enhanced insulin secretion.
- Glucose homeostasis and β-cell function were assessed in Gcg-deficient mice homozygous for a Gcg-GFP knock-in allele.
- Gcg(gfp/gfp) mice showed improved responses in oral and intraperitoneal glucose tolerance tests.
- Enhanced secretion of glucose-dependent insulinotropic polypeptide (GIP) was observed in response to glucose loads.
- Immunohistochemistry localized GIP to pancreatic β-cells in Gcg(gfp/gfp) mice.
- Ectopic GIP expression in β-cells may compensate for the absence of to maintain insulin secretion.
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Key numbers
2.8 to 16.7 mmol/L
Increased Insulin Secretion
Insulin secretion from islets was significantly higher in Gcg(gfp/gfp) mice.
5–6 mice per group
Improved Glucose Tolerance
Blood glucose levels during the OGTT in control and Gcg(gfp/gfp) mice.