Fatty acid synthase (FAS) regulation refers to the complex transcriptional, post-transcriptional, and allosteric control mechanisms that govern the activity of the Fatty Acid Synthase enzyme, a large multi-enzyme complex responsible for the de novo synthesis of long-chain fatty acids from acetyl-CoA and malonyl-CoA. Precise regulation of FAS is crucial for cellular lipid production, energy storage, and membrane biogenesis. Dysregulation is often observed in metabolic syndrome and certain cancers, reflecting an imbalance in energy homeostasis.
Origin
This term is rooted in fundamental biochemistry and metabolism, focusing on the enzyme that catalyzes a key step in lipogenesis. The concept of ‘regulation’ highlights the cellular and systemic controls exerted over this enzyme’s activity. In the context of hormonal health, FAS is a major target of endocrine signals like insulin and thyroid hormones, which promote lipogenesis in response to nutrient status, thereby linking hormonal signaling to energy storage and cellular structure.
Mechanism
The regulation is primarily achieved through gene expression modulated by transcription factors like Sterol Regulatory Element-Binding Protein 1c (SREBP-1c), which is activated by insulin signaling. Hormones such as insulin increase FAS expression, promoting the synthesis of saturated and monounsaturated fatty acids. Conversely, fasting and certain endocrine signals decrease its activity. Furthermore, allosteric regulation by long-chain fatty acyl-CoAs acts as a feedback loop, ensuring that the rate of fatty acid synthesis is tightly coupled to the body’s immediate metabolic needs and energy availability.
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