Cortisol receptor signaling
Glucocorticoid-driven lipolysis
Also searched as Glucocorticoid-driven lipolysis.
The balance here is the whole point, and it corrects a common assumption. In small rodents the fast nerve-and-adrenaline route dominates; in humans the slower endocrine route prevails, and this is one of its two named examples. So a product built only on the adrenaline story is built on the rodent version. But more is not better: the same steroids promote fat-cell enlargement and the growth of central fat depots, and are used in the laboratory precisely to make fat cells. It releases fat and builds the depot most people want smallest.
In depth
The stress-steroid route to fat release — slower than adrenaline, and in humans more important.
What drives it
Lowers cortisol increases it.
The HPA axis releases cortisol, the ligand that activates glucocorticoid-receptor signaling. PMID 7951523
What it drives
It increases Releases stored fat.
One of the two routes the human literature says prevails. 'Non-adrenergic lipolytic stimuli include glucocorticoids, natriuretic peptides, growth hormone, and TNF-alpha' (Endotext NBK555602 (NIH Bookshelf)). And the species point that matters most: 'in small rodents, rapid responses triggered by the SNS and the HPA axis seem to dominate; whereas in humans, endocrine regulation with a slower response time prevails, as exemplified by natriuretic peptides and glucocorticoids' (doi 10.1242/jeb.165381 [PMID 29514884]). The same source is candid that for these hormones 'the molecular mechanisms responsible for their lipolytic abilities have not been clearly elucidated.'. doi 10.1242/jeb.165381 · PMID 29514884
It increases Fat-cell formation↓.
It releases fat and builds the depot at the same time. 'GCs also promote adipocyte hypertrophy and differentiation of central fat depots that can lead to abdominal obesity and insulin resistance. In vitro adipogenesis studies include the wide use of the synthetic GC, dexamethasone' (Endotext nbk555602 (NIH Bookshelf)). The standard laboratory reagent for making fat cells is a glucocorticoid.
It increases Bone-building receptor.
Glucocorticoids upregulate PTH1R expression in osteoblastic cells. doi 10.1111/j.1601-0825.2006.01234.x · PMID 17241426
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.