Fatty acids are produced in the cytoplasm of cells by repeatedly adding two-carbon units to acetyl-CoA.
[4] After being packaged into VLDL in the liver, the resulting lipoprotein is then secreted directly into the blood for delivery to peripheral tissues.
Fatty acid synthesis starts with acetyl-CoA and builds up by the addition of two-carbon units.
VLDL particles are secreted directly into blood, where they function to deliver the endogenously derived lipids to peripheral tissues.
It is hypothesized that this effect occurs through the transcription factor SREBP-1, where the association of insulin and SREBP-1 lead to the gene expression of glucokinase.
It is involved in the process by limiting fat storage through inhibition of glucose intake and interfering with other adipose metabolic pathways.
[10] Through the promotion of fatty acid oxidation and lipogenesis inhibition, leptin was found to control the release of stored glucose from adipose tissues.
[13] There is also evidence suggesting that acylation stimulating protein (ASP) promotes the aggregation of triglycerides in adipose cells.
Glucagon has an antagonistic effect and increases phosphorylation, deactivation, thereby inhibiting ACC and slowing fat synthesis.
This rise activates AMP-activated protein kinase, which phosphorylates ACC and thereby inhibits fat synthesis.
SREBPs have been found to play a role with the nutritional or hormonal effects on the lipogenic gene expression.
[16] Overexpression of SREBP-1a or SREBP-1c in mouse liver cells results in the build-up of hepatic triglycerides and higher expression levels of lipogenic genes.