Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.
Lifestyle interventions and statins may target different components of the lipid profile, suggesting that they are not redundant strategies but could be combined for better benefits.
Loss of hepatic Cdk1 leads to oxidative stress, increased fatty acids in blood, and hyperinsulinemia, which resulted in insulin resistance and hepatic steatosis, similar as in diabetes.
Inhibition of C. elegans FLD-1 or Human TLCD1/2 prevents saturated fat lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.
A minor subset of plasma lipids are heritable, and this is associated with gene expression of transcripts related to roles beyond lipid metabolism, including immune function and cell signalling.
Lifelong HAO1 knockout was safe and without clinical phenotype in an identified healthy woman, de-risking a rare disease therapeutic approach through the power of naturally occurring human genetic variation.
LPCAT3 incorporates arachidonic acid into membrane phospholipids, which promotes lipoprotein assembly by enabling triacylgylcerols to cluster in the membrane.
