Abstract：
METHODS: Immunoglobulin A (IgA) selectively coats gut bacteria and contributes to regulatory functions in gastrointestinal inflammation and glucose metabolism. Excess intake of lard leads to decrease in the IgA coating of gut bacteria, although the underlying mechanisms remain unknown. This study validates how unabsorbed fat derived from a high-lard diet in the gut affects the IgA coating of bacteria, as assessed in mouse models using three types of dietary fat (lard, medium-, and long-chain triglycerides [MLCTs], and medium-chain triglycerides [MCTs]) exhibiting different digestibilities.
RESULTS: C57BL/6J mice are maintained on diets containing lard, MLCTs, or MCTs at 7% or 30% w/w for 10 weeks (n = 6 per group). The fecal fatty acid concentration is measured to quantify unabsorbed fat content. The ratio of IgA-coated bacteria to total bacteria (IgA coating ratio) in the feces is measured by flow cytometry. Compared to lard-fed mice, MLCT- and MCT-fed mice exhibit lower fecal concentrations of palmitic acid, stearic acid, and oleic acid and higher IgA coating ratios at both 7% and 30% dietary fat, and these parameters exhibit significant negative correlations.
CONCLUSIONS: Unabsorbed fat content in the gut may result in attenuated IgA coating of bacteria in high-lard diet-fed mice.
RESULTS: C57BL/6J mice are maintained on diets containing lard, MLCTs, or MCTs at 7% or 30% w/w for 10 weeks (n = 6 per group). The fecal fatty acid concentration is measured to quantify unabsorbed fat content. The ratio of IgA-coated bacteria to total bacteria (IgA coating ratio) in the feces is measured by flow cytometry. Compared to lard-fed mice, MLCT- and MCT-fed mice exhibit lower fecal concentrations of palmitic acid, stearic acid, and oleic acid and higher IgA coating ratios at both 7% and 30% dietary fat, and these parameters exhibit significant negative correlations.
CONCLUSIONS: Unabsorbed fat content in the gut may result in attenuated IgA coating of bacteria in high-lard diet-fed mice.
摘要：
方法：免疫球蛋白A（IgA）选择性包被肠道细菌，并有助于胃肠道炎症和葡萄糖代谢的调节功能。猪油的过量摄入导致肠道细菌的IgA涂层减少，尽管潜在的机制仍然未知。这项研究验证了肠道中来自高猪油饮食的未吸收脂肪如何影响细菌的IgA涂层，在小鼠模型中使用三种类型的膳食脂肪(猪油，medium-,和长链甘油三酯[MLCT]，和中链甘油三酯[MCT]）表现出不同的消化率。
结果：C57BL/6J小鼠维持含有猪油的饮食，MLCT,或MCT以7%或30%w/w持续10周(每组n=6)。测量粪便脂肪酸浓度以量化未吸收的脂肪含量。通过流式细胞术测量粪便中IgA包被的细菌与总细菌的比率(IgA包被比率)。与猪油喂养的老鼠相比，MLCT和MCT喂养的小鼠表现出较低的粪便浓度的棕榈酸，硬脂酸,和油酸和更高的IgA涂层比例在7%和30%的膳食脂肪，这些参数表现出显著的负相关关系。
结论：肠道中未吸收的脂肪含量可能导致高猪油饮食小鼠的细菌IgA涂层减弱。
结果：C57BL/6J小鼠维持含有猪油的饮食，MLCT,或MCT以7%或30%w/w持续10周(每组n=6)。测量粪便脂肪酸浓度以量化未吸收的脂肪含量。通过流式细胞术测量粪便中IgA包被的细菌与总细菌的比率(IgA包被比率)。与猪油喂养的老鼠相比，MLCT和MCT喂养的小鼠表现出较低的粪便浓度的棕榈酸，硬脂酸,和油酸和更高的IgA涂层比例在7%和30%的膳食脂肪，这些参数表现出显著的负相关关系。
结论：肠道中未吸收的脂肪含量可能导致高猪油饮食小鼠的细菌IgA涂层减弱。
