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Reduced hepatic AdipoR2 by increased glucocorticoid mediates effect of psychosocial stress to elevate serum cholesterol
Ist Teil von
Molecular and cellular endocrinology, 2024-10, Vol.592, p.112282-112282, Article 112282
Ort / Verlag
Ireland: Elsevier B.V
Erscheinungsjahr
2024
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
Understanding the effects of psychosocial stress on serum cholesterol may offer valuable insights into the relationship between psychological disorders and endocrine diseases. However, these effects and their underlying mechanisms have not been elucidated yet. Here we show that serum corticosterone, total cholesterol and low-density lipoprotein cholesterol (LDL-C) are elevated in a mouse model of psychosocial stress. Furthermore, alterations occur in AdipoR2-mediated AMPK and PPARα signaling pathways in liver, accompanied by a decrease in LDL-C clearance and an increase in cholesterol synthesis. These changes are further verified in wild-type and AdipoR2 overexpression HepG2 cells incubated with cortisol and AdipoR agonist, and are finally confirmed by treating wild-type and hepatic-specific AdipoR2 overexpression mice with corticosterone. We conclude that increased glucocorticoid mediates the effects of psychosocial stress to elevate serum cholesterol by inhibiting AdipoR2-mediated AMPK and PPARα signaling to decrease LDL-C clearance and increase cholesterol synthesis in liver.
•Serum cholesterol and GC elevate and liver AdipoR2 signaling alters in stressed mice.•AdipoR2 mediates cholesterol metabolism changes in GC-treated HepG2 cells.•GC alters mice serum cholesterol, liver AdipoR2 signaling and cholesterol metabolism.•AdipoR2 overexpression improves GC-induced changes in HepG2 cells and mice.