Research
Hormonal
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.
When you fast, your body switches to producing glucose and burning fat by turning on specific genes (via CREB and PGC1). This is a natural survival mechanism.
GoodSupportsHIGH confidence
Glucagon... induces a rise in intracellular cAMP... which in turn activates PKA... CREB is a ubiquitously expressed transcription factor that induces the expression of key genes involved in the gluconeogenesis pathway... The gene for the cofactor PGC1 is strongly activated by CREB in the liver... PGC1 was shown to increase the transcriptional activity mediated by both HNF4alpha and the glucocorticoid receptor bound to the PEPCK promoter.
Why this rating
Well-established molecular pathways described in a comprehensive review.
Source
Transcriptional Regulation of Metabolism
Béatrice Desvergne et al. · Physiological Reviews · 2006
DOI 10.1152/physrev.00025.2005
narrative_reviewCited 897×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- 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.Strong
- 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
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