Research
Macro partitioning
Inhibition of Acetyl-CoA Carboxylase 1 (ACC1) reduces de novo fatty acid synthesis and hepatic triglyceride accumulation, but may not sufficiently improve insulin sensitivity or fatty acid oxidation on its own compared to ACC2 inhibition.
Blocking the creation of new fat (via ACC1) reduces liver fat but does not fix insulin resistance or obesity on its own. The body compensates by trying to store fat elsewhere or failing to burn it. Effective treatment requires targeting ACC2 to ensure fat is actually burned, not just not made.
GoodQualifiesMEDIUM confidence
Under normal feeding conditions LACC1KO mice have no obvious health problems... LACC1KO mice fed a diet inducing obesity developed glucose intolerance and insulin resistance... antisense oligonucleotide against ACC1 reduced both fatty acid oxidation and fatty acid synthesis; because the malonyl-CoA level was basically unchanged, the exact effects of these inhibitors remain to be explored.
Why this rating
Supported by knockout mouse studies and antisense oligonucleotide trials, though results are more complex and less consistent than ACC2.
Source
Fatty acid metabolism: target for metabolic syndrome
Salih J. Wakil et al. · Journal of Lipid Research · 2008
narrative_reviewCited 724×
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