Obesity is associated with macrophage infiltration and low-grade inflammation, and it has been suggested that a diet high in cholesterol might exacerbate this inflammatory state. To evaluate whether dietary cholesterol has a negative impact on inflammation and atherosclerosis beyond what can be explained by obesity, Subramanian et al. exposed obese LDL-receptor-deficient mice to diabetogenic diets, either with or without adding dietary cholesterol to the diet. Both groups had a comparable body weight gain. However, in mice that ate the high-fat diet enriched with dietary cholesterol, insulin resistance, adipocyte hypertrophy, local inflammation, and circulating levels (and gene expression) of serum amyloid A were considerably increased compared to mice on the high-fat diet without addition of dietary cholesterol. Epididymal adipose tissue staining for macrophage infiltration revealed that mice with increased cholesterol intake had greater macrophage infiltration of adipose tissue, an observation that likely explains the relationship between increased cholesterol intake and increased inflammation-driven atherosclerosis.
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