Dietary Sphingomyelin Attenuates Inflammation and Metabolic Dysfunction in Diet‐ Induced Obese Mice

Abstract

Current evidence indicates that dietary sphingomyelin (SM) is lipid‐lowering and anti‐inflammatory, although its potential to prevent chronic disease as part of the diet has not been fully explored. SM is not a dietary essential and there is no recommended dietary intake. Consumption of dietary sphingolipids in Western diets is relatively common (0.3–0.4 g/day) and comes mainly from eggs and milk products. However, little is known about an optimal intake of SM and whether an increased dietary intake of SM is beneficial to health. Egg SM (ESM) and milk SM (MSM) differ in their fatty acid and sphingoid base composition, and may have different bioactivities when consumed in the diet. We evaluated the effects of milk and egg SM on diet‐induced obesity in high fat, high cholesterol diet‐fed C57BL/6J mice. We hypothesized that dietary SM would attenuate inflammation and metabolic dysfunction that occurs with obesity. We fed male C57BL/6J mice a high fat, high cholesterol diet (31% lard and 0.2% cholesterol by weight) (CTL; n = 14), or the same diet supplemented with either 0.1% (w/w) egg SM (ESM; n = 14) or 0.1% (w/w) milk SM (MSM; n = 13). After 10 weeks, ESM had gained significantly less weight than CTL reflected by a reduced epididymal adipose weight. ESM had significantly lower plasma cholesterol and fasting glucose when compared with the other groups. Although no significant difference was found in liver weight, H&E staining of both SM groups revealed an attenuation in the development of hepatic steatosis. Both SM groups had significantly lower plasma IFNγ and MCP‐1 compared to CTL. MSM also significantly lowered plasma TNFα, MIP‐1β, and IL‐6 compared to CTL. The reduction in inflammatory markers lead to an exploration of SM effects on macrophage activation. Milk SM significantly blunted LPS induction of both MCP‐1 and TNFα mRNA in RAW264.7 macrophages. These data suggest dietary SM has potential to influence obesity, through inhibiting lipid absorption and inflammation.Support or Funding InformationSupported by the University of Connecticut