Fatty acid synthase (FAS) complex regulation occurs primarily through transcriptional control, influenced by dietary signals and hormones like insulin.
Transcriptional Regulation of Fatty Acid Synthase
The primary method of FAS regulation is at the transcriptional level. This means the amount of FAS enzyme produced is controlled by regulating the gene that codes for it.
Key Regulators:
- Sterol Regulatory Element-Binding Protein-1c (SREBP-1c): This is a major transcription factor that activates the expression of the FAS gene. SREBP-1c is activated in response to high carbohydrate intake and insulin signaling.
- Upstream Stimulatory Factors (USFs): These transcription factors also play a role in regulating FAS gene expression.
Response to Feeding/Insulin:
When mammals are in a fed state, particularly after consuming carbohydrates, insulin levels rise. This leads to:
- Activation of SREBP-1c: Insulin promotes the processing and activation of SREBP-1c, allowing it to enter the nucleus and bind to the FAS gene promoter.
- Increased FAS Gene Transcription: SREBP-1c binding, along with USFs, stimulates the transcription of the FAS gene.
- Increased FAS Enzyme Production: More mRNA is produced, leading to increased synthesis of the FAS enzyme.
- Increased Fatty Acid Synthesis: With more FAS enzyme available, the rate of fatty acid synthesis increases.
Summary
Here is a table summarizing the regulatory factors for fatty acid synthase:
| Regulatory Factor | Mechanism of Action | Stimulus |
|---|---|---|
| SREBP-1c | Transcription factor; increases FAS gene expression | High carbohydrate intake, insulin |
| Upstream Stimulatory Factors (USFs) | Transcription factors; contribute to FAS gene expression | Feeding / Insulin |
Practical Implications
Understanding how FAS is regulated has implications for understanding and potentially treating metabolic disorders like obesity and type 2 diabetes. Manipulating the activity of SREBP-1c or FAS itself could be therapeutic targets.
