期刊
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 26, 期 8, 页码 868-875出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2015.03.005
关键词
Kaempferol; liver X receptor; Peroxisome proliferation-activated receptor; Sterol regulatory element-binding protein-1c; Lipid metabolism; Metabolic syndrome
资金
- National Research Foundation of Korea (NRF) - Korea government (MSIP) [2013R1A2A2A01016176]
Kaempferol is a dietary flavonol previously shown to regulate cellular lipid and glucose metabolism. However, its molecular mechanisms of action and target proteins have remained elusive, probably due to the involvement of multiple proteins. This study investigated the molecular targets of kaempferol. Ligand binding of kaempferol to liver X receptors (LXRs) was quantified by time-resolved fluorescence resonance energy transfer and surface plasmon resonance analyses. Kaempferol directly binds to and induces the transactivation of LXRs, with stronger specificity for the beta-subtype (EC50=033 mu M). The oral administration of kaempferol in apolipoprotein-E-deficient mice (150 mg/day/kg body weight) significantly reduced plasma glucose and increased high-density lipoprotein cholesterol levels and insulin sensitivity compared with the vehicle-fed control. Kaempferol also reduced plasma triglyceride concentrations and did not cause liver steatosis, a common side effect of potent LXR activation. In immunoblotting analysis, kaempferol reduced the nuclear accumulation of sterol regulatory element-binding protein-1 (SREBP-1). Our results show that the suppression of SREBP-1 activity and the selectivity for LXR-beta over LXR-alpha by kaempferol contribute to the reductions of plasma and hepatic triglyceride concentrations in mice fed kaempferol. They also suggest that kaempferol activates LxR-beta and suppresses SREBP-1 to enhance symptoms in metabolic syndrome. (C) 2015 Elsevier Inc. All rights reserved.
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