Dietary milk phospholipids increase body fat and modulate gut permeability, systemic inflammation, and lipid metabolism in mice.

The study examined how dietary milk polar lipids affect gut permeability, systemic inflammation, and lipid metabolism during diet-induced obesity (DIO). C57BL/6J mice (n = 6 × 3) were fed different diets with 34% fat as energy for 15 wk: (1) a modified AIN-93G diet (control; CO); (2) CO with milk gangliosides (GG); and (3) CO with milk phospholipids (MPL). Gut permeability was assessed by fluorescein isothiocyanate-dextran and sugar absorption tests. Intestinal tight junction proteins were evaluated by western blot. Plasma cytokines were measured by immunoassay. Body composition was assessed by magnetic resonance imaging. Tissue lipid profiles were obtained by thin layer chromatography. Hepatic expression of genes associated with lipid metabolism was assessed by real-time quantitative PCR. The MPL diet increased the efficiency of converting food into body fat and facilitated body fat accumulation compared with CO. The MPL and GG diets did not affect fasting glucose or the homeostasis model assessment of insulin resistance during DIO. The MPL diet increased and GG decreased plasma triglycerides compared with CO. The MPL diet decreased phospholipids subclasses in the muscle and increased those in the liver compared with CO. The GG and MPL diets had little effect on hepatic expression of genes associated with lipid metabolism. Compared with CO, the MPL diet decreased polar lipids content in colon mucosa. Small intestinal permeability decreased, whereas colon permeability increased and then recovered during the feeding period. High-fat feeding increased plasma endotoxin after DIO but did not affect plasma cytokines. The MPL and GG diets did not affect plasma endotoxin, adipokines, and inflammatory cytokines. After the establishment of obesity, MPL increased gut permeability to large molecules but decreased intestinal absorption of small molecules, whereas GG tended to have the opposite effects. The MPL and GG diets decreased mannitol and sucralose excretions, which peaked at d 45 in the CO group. The MPL diet decreased occludin in jejunum mucosa compared with CO. The GG and MPL diets did not affect zonula occludens-1 in gut mucosa. Overall, during DIO, milk GG decreased gut permeability, and had little effect on systemic inflammation and lipid metabolism; MPL facilitated body fat accumulation, decreased gut permeability, did not affect systemic inflammation.