| DOI | Trouver le DOI : https://doi.org/10.1016/j.ijcard.2013.03.057 |
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| Auteur | Rechercher : Li, Songtao; Rechercher : Li, Ying; Rechercher : Ning, Hua; Rechercher : Na, Lixin; Rechercher : Niu, Yucun; Rechercher : Wang, Maoqing; Rechercher : Feng, Rennan; Rechercher : Liu, Liyan; Rechercher : Guo, Fuchuan; Rechercher : Hou, Shaoying; Rechercher : Chu, Xia; Rechercher : Wang, Yemei; Rechercher : Zhang, Yunbo; Rechercher : Zhang, Huaqi; Rechercher : Huang, Lina; Rechercher : Bi, Mingxin; Rechercher : Huang, Yifan; Rechercher : Hao, Liuyi; Rechercher : Zhao, Yan; Rechercher : Wang, Cheng; Rechercher : Wang, Yanwen1; Rechercher : He, Yonghan1; Rechercher : Sun, Changhao |
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| Affiliation | - Conseil national de recherches du Canada. Développement des cultures et des ressources aquatiques
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| Format | Texte, Article |
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| Sujet | Calcium supplementation; Cholesterol; Estrogen; G-Protein coupled estrogen receptor |
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| Résumé | Background: Limited studies have addressed the effects of calcium supplementation (CaS) on serum total cholesterol (TC) in postmenopausal women and the results are inconclusive. Moreover, the potential mechanisms through which CaS regulates cholesterol metabolism in the absence of estrogen are still sealed for the limitation of human being study. Methods: Cross-sectional survey, animal and in vitro experiments were conducted to investigate the effect of CaS on endogenous cholesterol metabolism in estrogen deficiency and identify its potential mechanisms. Ovariectomized rats were used to mimic estrogen deficiency. In vitro, HepG2 cell line was exposed to estradiol and/or calcium treatment. Results: We demonstrated that CaS significantly increased serum TC and the risk of hypercholesterolemia and myocardial infarction in postmenopausal women. Increased serum TC in estrogen deficiency was caused mainly by decreased cholesterol catabolism rather than increased synthesis. This was mediated by reduced 7α-hydroxylase resulting from increased liver intracellular Ca²⁺ concentrations, reduced intracellular basal cAMP and subsequent up-regulation of SREBP-1c and SHP expression. Estrogen had a protective role in preventing CaS-induced TC increase by activating the G-protein coupled estrogen receptor, which mediated the estrogen effect through the transient receptor potential canonical 1 cation channel. Conclusions: CaS increases endogenous serum TC via decreasing hepatic cholesterol catabolism in estrogen deficiency. G-protein coupled estrogen receptor is shown to be a key target in mediating CaS-induced TC increase. CaS should be monitored for the prevention of serum TC increase during menopause. |
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| Date de publication | 2013-04-17 |
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| Dans | |
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| Langue | anglais |
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| Publications évaluées par des pairs | Oui |
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| Numéro du CNRC | NRCC 55825 |
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| Numéro NPARC | 21268659 |
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| Exporter la notice | Exporter en format RIS |
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| Signaler une correction | Signaler une correction (s'ouvre dans un nouvel onglet) |
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| Identificateur de l’enregistrement | ccb807c3-ff8e-46ff-9b6a-eea51d263619 |
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| Enregistrement créé | 2013-11-06 |
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| Enregistrement modifié | 2020-04-22 |
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