Prapa Ioanna, Yanni Amalia E, Kompoura Vasiliki, Mitropoulou Gregoria, Panas Panayiotis, Kostomitsopoulos Nikolaos, Kourkoutas Yiannis
Laboratory of Applied Microbiology and Biotechnology, Department of Molecular Biology and Genetics, Democritus University of Thrace, 68100 Alexandroupolis, Greece.
Laboratory of Chemistry, Biochemistry, Physical Chemistry of Foods, Department of Nutrition and Dietetics, Harokopio University of Athens, 17671 Athens, Greece.
Nutrients. 2024 Dec 6;16(23):4221. doi: 10.3390/nu16234221.
BACKGROUND/OBJECTIVES: The gut microbiota is linked to the pathogenesis of type 1 diabetes mellitus (T1DM), while supplementation with probiotics may result in positive alterations in the composition of the gut microbiome. This research aimed to map the changes in the gut microbiome and blood markers of streptozotocin-induced diabetic rats after a dietary intervention with free or immobilized cells of the presumptive probiotic SK on pistachio nuts.
Twenty-four male Wistar rats were studied and divided into four groups (healthy or diabetic) which received the free or the immobilized . SK cells on pistachio nuts for 4 weeks. Blood, fecal, and intestinal tissue samples were examined.
The diabetic rats exhibited an elevated concentration of HDL-c, while the inflammatory IL-1β levels were significantly lower in the diabetic animals that received the immobilized cells compared to the group that received the free cells. The dietary intervention with immobilized cells led to decreased counts of fecal staphylococci and enterococci in the diabetic animals, while the diet with both free and immobilized . SK cells rendered levels of these populations in normal values in the feces and intestinal tissue of the diabetic animals. Noticeably, the and genera were elevated after the supplementation with immobilized SK cells on pistachio nuts.
Dietary supplementation with SK cells (in free or in immobilized form) beneficially affected the gut microbiota/microbiome of streptozotocin-induced diabetic rats, leading to the alleviation of dysbiosis and inflammation and control over their lipid levels.
背景/目的：肠道微生物群与1型糖尿病（T1DM）的发病机制有关，而补充益生菌可能会使肠道微生物组的组成发生积极变化。本研究旨在描绘用开心果上自由或固定化的假定益生菌SK细胞进行饮食干预后，链脲佐菌素诱导的糖尿病大鼠肠道微生物组和血液标志物的变化。
对24只雄性Wistar大鼠进行研究，分为四组（健康或糖尿病组），分别接受开心果上自由或固定化的SK细胞，为期4周。对血液、粪便和肠道组织样本进行检测。
糖尿病大鼠的高密度脂蛋白胆固醇（HDL-c）浓度升高，而与接受自由细胞的组相比，接受固定化细胞的糖尿病动物体内炎症性白细胞介素-1β水平显著降低。用固定化细胞进行饮食干预导致糖尿病动物粪便中葡萄球菌和肠球菌数量减少，而自由和固定化SK细胞的饮食使糖尿病动物粪便和肠道组织中这些菌群的水平恢复正常。值得注意的是，在开心果上补充固定化SK细胞后，[具体菌属名称未给出]菌属增加。
用SK细胞（自由或固定化形式）进行饮食补充对链脲佐菌素诱导的糖尿病大鼠的肠道微生物群/微生物组产生有益影响，导致失调和炎症减轻，并控制其血脂水平。
