Effects of oral and intravenous fat load on blood pressure, endothelial function, sympathetic activity, and oxidative stress in obese healthy subjects

Aidar R Gosmanov, Dawn D Smiley, Gonzalo Robalino, Joselita Siquiera, Bobby Khan, Ngoc-Anh Le, Riyaz S Patel, Arshed A Quyyumi, Limin Peng, Abbas E Kitabchi, Guillermo E Umpierrez, Aidar R Gosmanov, Dawn D Smiley, Gonzalo Robalino, Joselita Siquiera, Bobby Khan, Ngoc-Anh Le, Riyaz S Patel, Arshed A Quyyumi, Limin Peng, Abbas E Kitabchi, Guillermo E Umpierrez

Abstract

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.

Figures

Fig. 1.
Fig. 1.
Changes in systolic blood pressure (BP; A), diastolic BP (B), flow-mediated dilatation (FMD; C), and heart rate (D) at 4 and 8 h after intravenous (iv) infusion of saline, intralipid, or oral fat load in obese subjects. Baseline systolic BP was 110 ± 3 mmHg. Baseline brachial artery diameter was 3.4 ± 0.11 mm. Values are means ± SE. †P < 0.05, *P < 0.01 compared with baseline.
Fig. 2.
Fig. 2.
Changes in plasma free fatty acids (FFA; A) and triglyceride (B) concentrations during the 8-h iv infusion of saline and intralipid or oral fat load in obese subjects. †P < 0.05, *P < 0.01 compared with baseline.
Fig. 3.
Fig. 3.
Thiobarbituric acid reactive substances (TBARS; A) and dicholorofluorescein (DCF; B) concentrations during the 8-h iv infusion of saline and intralipid or oral fat load in obese subjects. Values are means ± SE. †P < 0.05, *P < 0.01 compared with baseline.

Source: PubMed

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