Key result
While ADAM17 overexpression increases ACE2 shedding in vitro, ADAM17 does not deplete ACE2 from pancreatic islets in diabetic male db/db mice during disease progression.
Why the study?
Does ADAM17 deplete ACE2 levels in pancreatic islets and β-cells in diabetic mice?
Population
832/13 insulinoma cells and male db/db mice (8-, 12-, and 15-week-old) alongside nondiabetic db/m mice
Comparison
Overexpression of ADAM17 or inhibition of basal… vs Control cells or nondiabetic db/m mice
Design
Preclinical
Authors
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ACE2 gene therapy improves glucose regulation in diabetic mouse models; leaves open clinical translation and ADAM17 targeting in humans.
Does ADAM17 deplete ACE2 levels in pancreatic islets and β-cells in diabetic mice?
Although ADAM17 can shed ACE2 in vitro, it does not deplete ACE2 from pancreatic islets in diabetic db/db mice.
Pedersen et al. (2015) studied Diabetes. ADAM17 activity vs. Nondiabetic db/m mice or basal activity was evaluated on ACE2 shedding and cellular ACE2 levels. While ADAM17 overexpression increases ACE2 shedding in vitro, ADAM17 does not deplete ACE2 from pancreatic islets in diabetic male db/db mice during disease progression.
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