Emory University School of Medicine, Atlanta, GA 30303, USA.
Am J Physiol Endocrinol Metab. 2010 Dec;299(6):E953-8. doi: 10.1152/ajpendo.00469.2010. Epub 2010 Oct 5.
We compared the effects of high and low oral and intravenous (iv) fat load on blood pressure (BP), endothelial function, autonomic nervous system, and oxidative stress in obese healthy subjects. Thirteen obese subjects randomly received five 8-h infusions of iv saline, 20 (32 g, low iv fat) or 40 ml/h intralipid (64 g, high iv fat), and oral fat load at 32 (low oral) or 64 g (high oral). Systolic BP increased by 14 ± 10 (P = 0.007) and 12 ± 9 mmHg (P = 0.007) after low and high iv lipid infusions and by 13 ± 17 (P = 0.045) and 11 ± 11 mmHg (P = 0.040) after low and high oral fat loads, respectively. The baseline flow-mediated dilation was 9.4%, and it decreased by 3.8 ± 2.1 (P = 0.002) and 4.1 ± 3.1% (P < 0.001) after low and high iv lipid infusion and by 3.8 ± 1.8 (P = 0.002) and 5.0 ± 2.5% (P < 0.001) after low and high oral fat load, respectively. Oral and iv fat load stimulated oxidative stress, increased heart rate, and decreased R-R interval variability. Acute iv fat load decreased blood glucose by 6-10 mg/dl (P < 0.05) without changes in insulin concentration, whereas oral fat increased plasma insulin by 3.7-4.0 μU/ml (P < 0.01) without glycemic variations. Intravenous saline and both oral and iv fat load reduced leptin concentration from baseline (P < 0.01). In conclusion, acute fat load administered orally or intravenously significantly increased blood pressure, altered endothelial function, and activated sympathetic nervous system by mechanisms not likely depending on changes in leptin, glucose, and insulin levels in obese healthy subjects. Thus, fat load, independent of its source, has deleterious hemodynamic effects in obese subjects.
我们比较了高和低口服及静脉(iv)脂肪负荷对肥胖健康受试者血压(BP)、内皮功能、自主神经系统和氧化应激的影响。13 名肥胖受试者随机接受 5 次 8 小时静脉内生理盐水、20(32 克,低 iv 脂肪)或 40 毫升/小时脂肪乳剂(64 克,高 iv 脂肪)以及 32(低口服)或 64 克(高口服)的口服脂肪负荷。低和高 iv 脂质输注后收缩压分别增加 14±10(P=0.007)和 12±9mmHg(P=0.007),低和高口服脂肪负荷后分别增加 13±17(P=0.045)和 11±11mmHg(P=0.040)。基础血流介导的扩张率为 9.4%,低和高 iv 脂质输注后分别降低 3.8±2.1(P=0.002)和 4.1±3.1%(P<0.001),低和高口服脂肪负荷后分别降低 3.8±1.8(P=0.002)和 5.0±2.5%(P<0.001)。口服和 iv 脂肪负荷刺激氧化应激,增加心率,降低 R-R 间隔变异性。急性 iv 脂肪负荷使血糖降低 6-10mg/dl(P<0.05),而胰岛素浓度无变化,而口服脂肪使血浆胰岛素增加 3.7-4.0μU/ml(P<0.01),血糖无变化。静脉内生理盐水以及口服和 iv 脂肪负荷均使瘦素浓度从基线降低(P<0.01)。总之,口服或静脉内急性脂肪负荷显著增加肥胖健康受试者的血压,改变内皮功能,并通过不依赖于瘦素、血糖和胰岛素水平变化的机制激活交感神经系统。因此,脂肪负荷,与其来源无关,对肥胖受试者有有害的血液动力学影响。