A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance

作者:Bosse John D; Lin Han Yi; Sloan Crystal; Zhang Quan Jiang; Abel E Dale; Pereira Troy J; Dolinsky Vernon W; Symons J David; Jalili Thunder*
来源:American Journal of Physiology - Heart and Circulatory Physiology, 2013, 304(12): H1733-H1742.
DOI:10.1152/ajpheart.00631.2012

摘要

Previous studies reported that diets high in simple carbohydrates could increase blood pressure in rodents. We hypothesized that the converse, a low-carbohydrate/high-fat diet, might reduce blood pressure. Six-week-old spontaneously hypertensive rats (SHR; n = 54) and Wistar-Kyoto rats (WKY; n = 53, normotensive control) were fed either a control diet (C; 10% fat, 70% carbohydrate, 20% protein) or a low-carbohydrate/high-fat diet (HF; 20% carbohydrate, 60% fat, 20% protein). After 10 wk, SHR-HF had lower (P %26lt; 0.05) mean arterial pressure than SHR-C (148 +/- 3 vs. 159 +/- 3 mmHg) but a similar degree of cardiac hypertrophy (33.4 +/- 0.4 vs. 33.1 +/- 0.4 heart weight/tibia length, mg/mm). Mesenteric arteries and the entire aorta were used to assess vascular function and endothelial nitric oxide synthase (eNOS) signaling, respectively. Endothelium-dependent (acetylcholine) relaxation of mesenteric arteries was improved (P %26lt; 0.05) in SHR-HF vs. SHR-C, whereas contraction (potassium chloride, phenylephrine) was reduced (P %26lt; 0.05). Phosphorylation of eNOS(Ser1177) increased (P %26lt; 0.05) in arteries from SHR-HF vs. SHR-C. Plasma glucose, insulin, and homoeostatic model of insulin assessment were lower (P %26lt; 0.05) in SHR-HF vs. SHR-C, whereas peripheral insulin sensitivity (insulin tolerance test) was similar. After a 10-h fast, insulin stimulation (2 U/kg ip) increased (P %26lt; 0.05) phosphorylation of Akt(Ser473) and S6 in heart and gastrocnemius similarly in SHR-C vs. SHR-HF. In conclusion, a low-carbohydrate/high-fat diet reduced blood pressure and improved arterial function in SHR without producing signs of insulin resistance or altering insulin-mediated signaling in the heart, skeletal muscle, or vasculature.

  • 出版日期2013-6