Abstract
Western-style diets have been linked with dyslipidemia and inflammation, two well-known risk factors associated with cardiovascular disease (CVD). Dietary sphingomyelin (SM) has been reported to modulate gut microbiota, and lower serum lipids and inflammation in mice on Western-style diets. However, few studies have examined if nutritionally-relevant intake of dietary SM can impact atherosclerosis progression. Thus, the aim of this study was to determine if incorporating 0.1% (w/w) egg SM (ESM) (equivalent to ~750 mg/day in humans) into a high-fat (45% kcal), cholesterol-enriched diet (HFD) could prevent atheroprogression in apoE−/− mice (n = 15/group). We found that mice fed with the ESM-rich diet had significantly lower epididymal fat mass (−46%) and tended to have higher spleen weights (+15%). There were no significant differences in serum lipids between groups. However, ESM-fed mice had significantly lower alanine aminotransferase (ALT) activity. Additionally, ESM-fed mice displayed significantly less aortic root lipid accumulation (−31%) compared to controls. This improvement in atherosclerosis was paired with over a two-fold reduction in circulating serum amyloid A (SAA) in ESM-fed mice. Finally, there was also a modulation of the gut microbiota with ESM supplementation. ESM may have the potential to prevent atherosclerosis, however further research in the clinical setting is warranted.
Highlights
Cardiovascular disease (CVD) is the leading cause of non-communicable deaths in the UnitedStates [1]
egg SM (ESM) was fed at a 1:2 mass ratio of cholesterol in the diets, which is similar to the ratio found in egg yolk [26,27]
ApoE−/− mice were fed a HFD with added cholesterol supplemented with or without 0.1% ESM—the latter contained a mass ratio of 2:1 cholesterol/SM that mimics the ratio in egg yolk
Summary
Cardiovascular disease (CVD) is the leading cause of non-communicable deaths in the United. This disease is not confined to the U.S alone. 35% of deaths can be attributed to CVD, reinforcing the importance of addressing the etiology of this disease [2]. Atherosclerosis is a prominent contributor of CVD, which is characterized by the accumulation of lipids, cholesterol, in the arterial wall and eventually leads to lesion development [3]. Atherosclerosis development is enhanced by both disordered lipid metabolism and chronic inflammation. If the lipid load becomes unmanageable, foam cell formation and lesion development occur, which can result in an inflammatory plaque environment [4]
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