Abstract
Vegetable oils such as palm oil (enriched in saturated fatty acids, SFA) and high-oleic-acid sunflower oil (HOSO, containing mainly monounsaturated fatty acids, MUFA) have emerged as the most common replacements for trans-fats in the food industry. The aim of this study is to analyze the impact of SFA and MUFA-enriched high-fat (HF) diets on endothelial function, vascular remodeling, and arterial stiffness compared to commercial HF diets. Five-week-old male C57BL6J mice were fed a standard (SD), a HF diet enriched with SFA (saturated oil-enriched Food, SOLF), a HF diet enriched with MUFA (unsaturated oil-enriched Food, UOLF), or a commercial HF diet for 8 weeks. Vascular function was analyzed in the thoracic aorta. Structural and mechanical parameters were assessed in mesenteric arteries by pressure myography. SOLF, UOLF, and HF diet reduced contractile responses to phenylephrine and induced endothelial dysfunction in the thoracic aorta. A significant increase in the β-index, and thus in arterial stiffness, was also detected in mesenteric arteries from the three HF groups, due to enhanced deposition of collagen in the vascular wall. SOLF also induced hypotrophic inward remodeling. In conclusion, these data demonstrate a deleterious effect of HF feeding on obesity-related vascular alterations that is exacerbated by SFA.
Highlights
Obesity constitutes one of the major preventable risk factors for the development of several noncommunicable diseases including cardiovascular alterations, diabetes, musculoskeletal disorders, and some cancers [1]
After one week of acclimation, animals were randomly divided into four groups (n = 7–10) with a similar average body weight (BW) and assigned to a standard diet (SD, 18% energy from fat; Harlan Laboratories, España, Spain), a HF diet enriched in saturated fat, a HF diet enriched in monounsaturated fat, or a commercially available high-fat diet (HF, 62% energy from fat, Test Diets, UK) for 8 weeks
The novel findings of this study are that UOLF, as well as SOLF and HF diets impair endothelial function and increase arterial stiffness as a result of enhanced collagen deposition in the arterial wall
Summary
Obesity constitutes one of the major preventable risk factors for the development of several noncommunicable diseases including cardiovascular alterations, diabetes, musculoskeletal disorders, and some cancers [1]. In both humans and mice models, increasing evidence has shown that obesity favors the development of vascular damage, such as endothelial dysfunction, that seems to be due, at least in part, to compromised nitric oxide (NO) availability [2,3] and/or increased oxidative stress [3,4]. In addition to endothelial dysfunction, the two other crucial mechanisms implicated in vascular alterations are arterial remodeling and stiffness. We have recently demonstrated that extracellular matrix remodeling, including an increase in collagen content and elastin fragmentation, plays a key role in the development of central arterial stiffness due to obesity [7]
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