API
Event: 89
Key Event Title
Short name
Synthesis, De Novo FABiological Context
| Level of Biological Organization |
|---|
| Cellular |
Cell term
| Cell term |
|---|
| hepatocyte |
Organ term
Key Event Components
| Process | Object | Action |
|---|---|---|
| fatty acid biosynthetic process | fatty acid | increased |
Key Event Overview
AOPs Including This Key Event
| AOP Name | Role of event in AOP |
|---|---|
| LXR Activation to Liver Steatosis | KeyEvent |
Stressors
Taxonomic Applicability
Life Stages
Sex Applicability
Key Event Description
A number of pathways and a great number of enzymes like GK, L-PK, ACC, FAS and SCD-1 are involved in the de novo FA synthesis [1]. As it is already discussed above these enzymes are induced by LXR agonists (FAS, SCD1), the SREBP-1c (GK, ACC, FAS) and the ChREBP (L-PK, ACC, FAS) leading to enhancement of the de novo FA synthesis.
Figure 1. Metabolic pathway for de novo FA synthesis and TG formation [1]
As proposed from Diraison et al 1997 the de novo FA synthesis contributes maximum 5% to the synthesis of FA and TG under normal conditions. Conditions associated with high rates of lipogenesis, such as low fat - high carbohydrate (LF/HC) diet, hyperglycemia, and hyperinsulinemia are associated with a shift in cellular metabolism from lipid oxidation to TG esterification, thereby increasing the availability of TGs derived from VLDL synthesis and secretion.