Key result
In HepG2 cells, the majority of newly synthesized triglyceride is rapidly shifted to a cytoplasmic pool that does not regulate apolipoprotein B secretion, explaining low secretion rates.
Population
HepG2 cells
Design
Preclinical
Authors
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HepG2 data warrant caution extrapolating to human apoB regulation; leaves open triglyceride routing in primary hepatocytes.
In HepG2 cells, low rates of apolipoprotein B secretion result from the preferential routing of newly synthesized triglycerides to a non-secretory cytoplasmic pool rather than a secretion-coupled microsomal pool.
Wu et al. (1996) studied HepG2 cells. Oleic acid and Dibutyryl cAMP was evaluated on Apolipoprotein B secretion and intracellular triglyceride pools. In HepG2 cells, the majority of newly synthesized triglyceride is rapidly shifted to a cytoplasmic pool that does not regulate apolipoprotein B secretion, explaining low secretion rates.
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