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Event: 89
Key Event Title
Synthesis, De Novo FA
Short name
Biological 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 | Point of Contact | Author Status | OECD Status |
---|---|---|---|---|
LXR Activation to Liver Steatosis | KeyEvent | Agnes Aggy (send email) | Not under active development |
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.