β-estradiol adjusts intestinal function via ERβ and GPR30 mediated PI3K/AKT signaling activation to alleviate postmenopausal dyslipidemia.
Animals
Apolipoproteins E
/ genetics
Caco-2 Cells
Dyslipidemias
/ blood
Estradiol
/ administration & dosage
Estrogen Receptor beta
/ metabolism
Estrogens
/ administration & dosage
Female
Humans
Jejunum
/ drug effects
Lipids
/ blood
Mice
Mice, Inbred C57BL
Mice, Knockout, ApoE
Ovariectomy
Phosphatidylinositol 3-Kinases
/ metabolism
Postmenopause
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
Receptors, Estrogen
/ metabolism
Receptors, G-Protein-Coupled
/ metabolism
Signal Transduction
Dyslipidemia
Estradiol
Estrogen receptor
Intestine
Postmenopause
Journal
Biochemical pharmacology
ISSN: 1873-2968
Titre abrégé: Biochem Pharmacol
Pays: England
ID NLM: 0101032
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
19
05
2020
revised:
30
06
2020
accepted:
01
07
2020
pubmed:
7
7
2020
medline:
12
1
2021
entrez:
7
7
2020
Statut:
ppublish
Résumé
Decreases in estrogen secretion and estrogen receptor function lead to an increase in the incidence of dyslipidemia and cardiovascular disease (CVD) in postmenopausal women. We previously reported that β-estradiol has a significant regulatory effect on lipids in ApoE
Identifiants
pubmed: 32628929
pii: S0006-2952(20)30370-1
doi: 10.1016/j.bcp.2020.114134
pii:
doi:
Substances chimiques
Apolipoproteins E
0
Estrogen Receptor beta
0
Estrogens
0
GPER1 protein, mouse
0
Lipids
0
Receptors, Estrogen
0
Receptors, G-Protein-Coupled
0
Estradiol
4TI98Z838E
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
114134Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.