title: A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance.
abstract: 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 < 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 < 0.05) in SHR-HF vs. SHR-C, whereas contraction (potassium chloride, phenylephrine) was reduced (P < 0.05). Phosphorylation of eNOSSer1177 increased (P < 0.05) in arteries from SHR-HF vs. SHR-C. Plasma glucose, insulin, and homoeostatic model of insulin assessment were lower (P < 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 < 0.05) phosphorylation of AktSer473 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.
authors.affiliation: Division of Nutrition, University of Utah, Salt Lake City, UT 84112, USA.
authors.forename: John D
authors.initials: JD
authors.lastname: Bosse
authors.forename: Han Yi
authors.initials: HY
authors.lastname: Lin
authors.forename: Crystal
authors.initials: C
authors.lastname: Sloan
authors.forename: Quan-Jiang
authors.initials: QJ
authors.lastname: Zhang
authors.forename: E Dale
authors.initials: ED
authors.lastname: Abel
authors.forename: Troy J
authors.initials: TJ
authors.lastname: Pereira
authors.forename: Vernon W
authors.initials: VW
authors.lastname: Dolinsky
authors.forename: J David
authors.initials: JD
authors.lastname: Symons
authors.forename: Thunder
authors.initials: T
authors.lastname: Jalili
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology / Q000502:physiology; D001786:Blood Glucose; D001794:Blood Pressure; D006332:Cardiomegaly / Q000178:diet therapy; D050528:Diet, Carbohydrate-Restricted; D059305:Diet, High-Fat; D004730:Endothelium, Vascular / Q000378:metabolism; D006973:Hypertension / Q000178:diet therapy*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008638:Mesenteric Arteries / Q000166:cytology / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010766:Phosphorylation; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D014664:Vasodilation
chemical_list: D001786:Blood Glucose; D007328:Insulin; D052250:Nitric Oxide Synthase Type III
keywords: arterial function; blood pressure; diet; heart; hypertrophy