Key result
ACE2 deficiency increased lipid accumulation and ER stress in skeletal muscle, while ACE2 overexpression ameliorated these effects and improved mitochondrial function via the IKKβ/NFκB/IRS-1 pathway.
Why the study?
The role of ACE2 in regulating ER stress and mitochondrial function to prevent intramuscular fat accumulation was not clear.
Population
ACE2 knockout mice, Ad-ACE2-treated db/db mice, and ACE2-overexpression C2C12 cells
Comparison
ACE2 deficiency and Ad-ACE2 treatment vs controls
Design
Preclinical animal and cell study
Authors
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May warrant preclinical validation of ACE2 modulation for muscle metabolism; leaves open human cardiometabolic translation.
p-value: p=<0.05
ACE2 plays a notable role in regulating intramuscular fat by improving endoplasmic reticulum and mitochondrial function, providing a potential strategy for treating insulin resistance in skeletal muscle.
Cao et al. (2019) studied Intramuscular fat accumulation and insulin resistance. ACE2 modulation (knockout or overexpression) vs. Wild-type mice or Ad-GFP control was evaluated on Intramuscular triglyceride content and expression of lipid metabolism, ER stress, and mitochondrial function genes (p=<0.05). ACE2 deficiency increased lipid accumulation and ER stress in skeletal muscle, while ACE2 overexpression ameliorated these effects and improved mitochondrial function via the IKKβ/NFκB/IRS-1 pathway.
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