Propionate Helps Heart Function in Mice Lacking Akt2
Author Information
Author(s): Li Linlin, Hua Yinan, Ren Jun
Primary Institution: University of Wyoming
Hypothesis
This study examines the effect of Akt2 knockout on cardiomyocyte dysfunction and the impact of propionate treatment on these responses.
Conclusion
Propionate treatment alleviated cardiac contractile and mitochondrial dysfunction caused by Akt2 knockout in mice.
Supporting Evidence
- Akt2 knockout mice showed glucose intolerance and compromised heart cell function.
- Propionate treatment improved heart cell contractile function in Akt2 knockout mice.
- Mitochondrial membrane potential loss in Akt2 knockout mice was restored by propionate.
Takeaway
When mice were missing a specific protein called Akt2, their heart cells didn't work well. Giving them a substance called propionate helped their hearts work better.
Methodology
Adult male wild-type and Akt2 knockout mice were treated with propionate or vehicle for 7 days, followed by assessments of glucose tolerance, cardiomyocyte function, and protein expression.
Limitations
The study was conducted in mice, which may not fully represent human physiology.
Participant Demographics
Adult male mice aged 5-6 months.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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