食用富含饱和脂肪的饮食会增加肠道对脂质的吸收，组装成乳糜微粒，并通过淋巴和循环系统输送到代谢组织。由鞘氨醇和脂肪酸组成的神经酰胺脂质在代谢组织中的积累有助于心血管疾病、2 型糖尿病和癌症的发病机制。使用肠系膜淋巴管插管的大鼠模型，我们发现神经酰胺由肠道产生并组装成乳糜微粒，乳糜微粒通过肠系膜淋巴系统运输。对肠道来源的乳糜微粒进行脂质组学筛选，发现了以前在乳糜微粒中未检测到的多种脂肪酸、鞘脂和甘油脂种类，包括对代谢有害的 C16:0 神经酰胺，其在大鼠和小鼠中因高脂肪喂养而增加。人类高脂代餐肠内喂养。总之，高脂肪喂养增加了乳糜微粒中肠源性 C16:0 神经酰胺的输出，确定了一种潜在的未知机制，神经酰胺通过该机制进行全身转运，从而导致代谢功能障碍。

Consumption of a diet rich in saturated fat increases lipid absorption from the intestine, assembly into chylomicrons, and delivery to metabolic tissues via the lymphatic and circulatory systems. Accumulation of ceramide lipids, composed of sphingosine and a fatty acid, in metabolic tissues contributes to the pathogenesis of cardiovascular diseases, type 2 diabetes mellitus and cancer. Using a mesenteric lymph duct cannulated rat model, we showed that ceramides are generated by the intestine and assembled into chylomicrons, which are transported via the mesenteric lymphatic system. A lipidomic screen of intestinal-derived chylomicrons identified a diverse range of fatty acid, sphingolipid, and glycerolipid species that have not been previously detected in chylomicrons, including the metabolically deleterious C16:0 ceramide that increased in response to high-fat feeding in rats and human high-lipid meal replacement enteral feeding. In conclusion, high-fat feeding increases the export of intestinal-derived C16:0 ceramide in chylomicrons, identifying a potentially unknown mechanism through which ceramides are transported systemically to contribute to metabolic dysfunction.