A High-Lipid Diet Potentiates Left Ventricular Dysfunction in Nitric Oxide Synthase 3-Deficient Mice after Chronic Pressure Overload  

Oleh:

Ahmadie, Roien ; Santiago, Jon-Jon ; Walker, Jonathan

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 140 no. 08 (Aug. 2010), page 1438-1444.
Topik: Left Ventricular Dysfunction

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

A high-lipid diet (HLD) may lead to adverse left ventricular (LV) remodeling and endothelial dysfunction in conditions of hemodynamic stress. Although congenital absence of nitric oxide synthase 3 (NOS3) leads to adverse LV remodeling after transverse aortic constriction (TAC), the effects of a HLD in this state remains unknown. Wild-type (WT) and NOS3 knockout mice (NOS3-/-) were randomized into the following 4 groups: 1) WT + low-lipid diet (LLD) (10% of energy); 2) WT + HLD (60% of energy); 3) NOS3-/- + LLD; and 4) NOS3-/- + HLD for a total of 12 wk. After 1 wk of randomization, TAC was performed on all groups. Serial echocardiography revealed a decrease in LV ejection fraction (LVEF) in WT and NOS3-/- mice fed the HLD compared with those fed the LLD diet at 12 wk post-TAC. Mice fed the NOS3-/- + HLD diet had a lower LVEF compared with mice in the other 3 groups (P < 0.05). There was greater myocyte hypertrophy, interstitial fibrosis, and percentage change in plasma cholesterol concentrations in the NOS3-/- + HLD group 12 wk post-TAC compared with the other 3 groups. Although high molecular weight fibroblast growth factor-2, a marker of cardiac hypertrophy, was more upregulated in the NOS3-/- + HLD group than in the other groups, markers of the renin-angiotensin system did not differ among them. A HLD potentiates LV dysfunction in NOS3-/- mice in a chronic pressure overload state.

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