Hormonal
Transcriptional regulation by nuclear receptors (specifically PPARs, LXRs, and SREBPs) and transcription factors (ChREBP, FOXOs) serves as the primary long-term mechanism for maintaining metabolic homeostasis by coordinating glucose, lipid, and amino acid metabolism in response to fasting and feeding cycles.
Your body doesn't just burn calories; it actively reprograms its genes based on your diet to manage energy. High glucose and insulin trigger genes for fat storage (via SREBP-1c and ChREBP), while fasting and glucagon trigger genes for fat burning and glucose production (via PPARs and FOXOs). Understanding this helps explain why extreme diets can alter metabolic efficiency long-term.
It is now commonly accepted that metabolic regulation in complex organisms relies on three main types of control... The third mechanism is transcriptional regulation, which affects the level of expression of key enzymes and is effective on a longer time scale. It clearly appears that most metabolic regulations benefit from a coordination of these various mechanisms.
Why this rating
This is a comprehensive review in a high-impact journal (Physiological Reviews) summarizing decades of molecular biology research.
Source
Transcriptional Regulation of Metabolism
Béatrice Desvergne et al. · Physiological Reviews · 2006
DOI 10.1152/physrev.00025.2005
More from this paper
- Insulin signaling promotes lipid synthesis and glucose storage by upregulating SREBP-1c and ChREBP, while simultaneously repressing gluconeogenic genes via the inhibition of FOXO transcription factors.Strong
- High glucose levels independently regulate gene expression through the transcription factor ChREBP, which is activated by glucose metabolites (xylulose 5-phosphate) to promote lipogenesis and glycolysis, even in the absence of insulin.Good
- Fasting and low glucose levels trigger transcriptional changes that promote gluconeogenesis and fatty acid oxidation via the activation of transcription factors like CREB, PGC1, and PPARs, counteracting insulin's effects.Good
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