ncbi.nlm.nih.gov/m/pubmed/10856…
It includes details on cholesterol esterification, intracellular TG accumulation and ApoB secretion.
1-Why does C14 and sometimes C12 appear potent in clinical feeding studies, despite being so weak in promoting ApoB secretion in vitro?
C14 and C12 probably increase LDL-C by other mechanisms different from C16, or probably, these fatty acids are elongated in vivo.
The second question, why does unsaturated greatly increase ApoB in vitro, but lower it in vivo?