Key result
Intrapancreatic injection of an adenovirus encoding human ACE2 significantly reduced fasting blood glucose (167.8 vs 212.3 mg/dl) and improved glucose tolerance in angiotensin II-infused mice.
Why the study?
Does pancreatic ACE2 overexpression improve glycemia and beta-cell function in Angiotensin II-infused mice?
Does pancreatic ACE2 overexpression improve glycemia and beta-cell function in Angiotensin II-infused mice?
Absolute Event Rate: 167.8% vs 212.3%
p-value: p=<0.05
Pancreatic ACE2 overexpression restores β-cell function and improves glycemia in a mouse model of Angiotensin II-induced hyperglycemia, suggesting a potential therapeutic target for diabetes associated with an overactive renin-angiotensin system.
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Pancreatic ACE2 overexpression may improve glycemia in Ang II-infused mice; leaves open translation to human diabetes with RAS overactivity.
Chhabra et al. (2013) studied Angiotensin II-induced hyperglycemia (n=82). Adenovirus encoding human ACE2 (Ad-hACE2) vs. Control adenovirus (Ad-eGFP) was evaluated on Fasting blood glucose at 14 days (mg/dl) (p=<0.05). Intrapancreatic injection of an adenovirus encoding human ACE2 significantly reduced fasting blood glucose (167.8 vs 212.3 mg/dl) and improved glucose tolerance in angiotensin II-infused mice.
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