000			nab a22 7a 4500
999			_c17061 _d17061
003			PC17061
005			20221114101652.0
008			221114b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_92167 _aRuiz Hurtado, Gema _eInstituto de Investigación i+12
245	0	0	_aHigh-fat diet induces endothelial dysfunction through a down-regulation of the endothelial AMPK-PI3K-Akt-eNOS pathway. _h[artículo]
260			_bMolecular nutrition & food research, _c2015
300			_a59(3):520-32.
500			_aFormato Vancouver: García Prieto CF, Hernández Nuño F, Rio DD, Ruiz Hurtado G, Aránguez I, Ruiz Gayo M et al. High-fat diet induces endothelial dysfunction through a down-regulation of the endothelial AMPK-PI3K-Akt-eNOS pathway. Mol Nutr Food Res. 2015 Mar;59(3):520-32.
501			_aPMID: 25421217
504			_aContiene 48 referencias
520			_aScope: Activation of endothelial adenosine monophosphate-activated protein kinase (AMPK) contributes to increase nitric oxide (NO) availability. The aim of this study was to assess if high-fat diet (HFD)-induced endothelial dysfunction is linked to AMPK deregulation. Methods and results: Twelve-week-old Sprague Dawley male rats were assigned either to control (10 kcal % from fat) or to HFD (45 kcal % from fat) for 8 wk. HFD rats segregated in obesity-prone (OP) or obesity-resistant (OR) rats according to body weight. HFD triggered an impaired glucose management together with impaired endothelium-dependent relaxation, reduced endothelial AMPK activity and lower NO availability in aortic rings of OP and OR cohorts. Relaxation evoked by AMPK activator, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) was reduced in both OP and OR rings, which exhibited lower p-AMPKα-Thr(172) /AMPKα ratios that negatively correlated with plasma non-esterified fatty acids (NEFA) and triglycerides (TG). Inhibition of PI3K (wortmannin, 10(-7) M) or Akt (triciribine, 10(-5) M) reduced relaxation to AICAR only in the control group (p < 0.001). Akt (p-Akt-Ser(473) ) and eNOS phosphorylation (p-eNOS-Ser(1177) ) were significantly reduced in OP and OR (p < 0.01). Conclusion: Endothelial dysfunction caused by HFD is related to a dysfunctional endothelial AMPK-PI3K-Akt-eNOS pathway correlating with the increase of plasma NEFA, TG, and an impaired glucose management.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc17061.pdf _ySolicitar documento
942			_2ddc _cART _n0