Effect of High-Fat Diet upon Inflammatory Markers and Aortic Stiffening in Mice

Abstract

Changes in lifestyle such as increase in high-fat food consumption are an important cause for vascular diseases. The present study aimed to investigate the involvement of ACE and TGF-β in the aorta stiffness induced by high-fat diet. C57BL/6 male mice were divided in two groups according to their diet for 8 weeks: standard diet (ST) and high-fat diet (HF). At the end of the protocol, body weight gain, adipose tissue content, serum lipids and glucose levels, and aorta morphometric and biochemical measurements were performed. Analysis of collagen fibers by picrosirius staining of aorta slices showed that HF diet promoted increase of thin (55%) and thick (100%) collagen fibers deposition and concomitant disorganization of these fibers orientations in the aorta vascular wall (50%). To unravel the mechanism involved, myeloperoxidase (MPO) and angiotensin I converting enzyme (ACE) were evaluated by protein expression and enzyme activity. HF diet increased MPO (90%) and ACE (28%) activities, as well as protein expression of ACE. TGF-β was also increased in aorta tissue of HF diet mice after 8 weeks. Altogether, we have observed that the HF diet-induced aortic stiffening may be associated with increased oxidative stress damage and activation of the RAS in vascular tissue.

Regional variation in arterial stiffening and dysfunction in Western diet-induced obesity

“…Re-cent studies have described a number of specific processes underlying obesity-associated aortic stiffening and increased PWV, including intima-medial thickening with fibrosis (13), medial (i.e., smooth muscle) hypertrophy with increased extracellular matrix cross-linking (48), and increased aortic collagen content and disorganization (37). Consistent with other reports, these changes often occur in concert with obesityassociated aortic endothelial dysfunction and inflammation (38,48).…”

β2-Adrenoceptors Antiarrhythmic Effects in Wild Type Mice Fed a Cholesterol-Enriched Diet

“…Fat intake promotes significant structural changes in arterial walls, particularly through activation of the renin-angiotensin system, induction of oxidative stress and proinflammatory factors [4,5]. Those changes in conductance vessels constitute a risk for cardiovascular diseases [19]. LDLr-/-mice fed the same cholesterol-enriched diet that was used here developed dyslipidemia, atherosclerosis, left ventricular hypertrophy, high mean arterial pressure and reduced cardiac contractility [15].…”

Dietary Interventions, Cardiovascular Aging, and Disease

“…11,12 Increased intake of high-fat foods directly affects this homeostasis and contributes to vascular diseases by promoting major changes in arterial tissue, especially through the activation of renin-angiotensin system and the induction of oxidative stress and proinflammatory factors. 13 The HFD promotes increased disorganization of collagen fiber in the vascular wall of the aorta and induces aortic stiffening partly by elevating oxidative stress damage and activating renin-angiotensin system in vascular tissue. 13 A variation of the HFD, called the Paigen diet, can also induce CVDs-associated damage in murine models.…”

“…13 The HFD promotes increased disorganization of collagen fiber in the vascular wall of the aorta and induces aortic stiffening partly by elevating oxidative stress damage and activating renin-angiotensin system in vascular tissue. 13 A variation of the HFD, called the Paigen diet, can also induce CVDs-associated damage in murine models. This diet was developed in 1985 by combining the atherogenic ThomasHartroft diet, 14 which contains 30% cocoa butter (primarily saturated fats) with Purina breeder chow, which contains 10% fat.…”