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Bifidobacterium pseudocatenulatum CECT 7765 reverses the adverse effects of diet-induced obesity through the gut-bone axis

机译:双歧杆菌PseudocateNulatum Cect 7765通过肠骨轴逆转饮食诱导的肥胖症的不利影响

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Obesity and the associated chronic metabolic diseases (e.g., type-2 diabetes) adversely affect bone metabolism and health. Gut microbiota is considered to be involved in the pathophysiology of obesity and also represents a therapeutic target. This study has investigated the contribution of diet-induced obesity to alterations in bone health and metabolism and whether these could be restored by oral administration of Bifidobacterium pseudocatenulatum CECT 7765. To do so, adult male wild-type C57BL-6 mice were fed either a standard or high-fat diet (HFD), supplemented or not with B. pseudocatenulatum CECT 7765 (109 CFU/day) for 14 weeks. Effects on bone mass density (BMD), bone mineral content, bone remodeling, bone structure and gene expression were assessed. In HFD-fed mice, bone microstructural properties at the distal femur showed deteriorated trabecular architecture in bone volumetric fraction, trabecular number and trabecular pattern factor. Besides, the HFD reduced the volumetric bone mineral density in the trabecular bone, but not in the cortical bone. All these bone microstructural alterations found in obese mice were reversed by B. pseudocatenulatum CECT 7765. Administration of the bacterium increased (p < .05) the Wnt/beta-catenin pathway gene expression, which could mediate effects on BMD. Bifidobacterium pseudocatenulatum CECT 7765 supplementation increased (p < .05) serum osteocalcin (OC, bone formation parameter), and decreased serum C-terminal telopeptide (CTX) (p < .01) and parathormone (PTH) (p < .05) (both bone resorption parameters). It also altered the microstructure of the femur. In summary, HFD interfered with the normal bone homeostasis leading to increased bone loss. In obese mice, B. pseudocatenulatum CECT 7765 lowered bone mass loss and enhanced BMD by decreasing bone resorption and increasing bone formation.
机译:肥胖症和相关的慢性代谢疾病(例如,2型糖尿病)对骨代谢和健康产生不利影响。肠道微生物会被认为参与肥胖症的病理生理学,也代表了治疗目标。本研究研究了饮食诱导的肥胖对骨骼健康和新陈代谢的改变的贡献,以及这些是否可以通过双歧杆菌的口服施用7765来恢复。这样做,成年雄性野生型C57BL-6小鼠被喂食A.标准或高脂饮食(HFD),补充或不含B.PseudocateNulatum Cect 7765(109 CFU /日),为14周。评估对骨质量密度(BMD),骨矿物质含量,骨重塑,骨结构和基因表达的影响。在HFD喂养小鼠中,远端股骨的骨微观结构性质在骨体积分数,颌骨数和小梁图案因子中显示出劣化的小梁架构。此外,HFD降低了小梁骨中的体积骨密度,但不在皮质骨中。在肥胖小鼠中发现的所有这些骨骼微观结构改变由B.PseudocateNulatum Cect 7765逆转。施用细菌(p <.05)Wnt /β-连环蛋白途径基因表达,其可以介导对BMD的影响。双歧杆菌pseudocateNulatum cect 7765补充(p <.05)血清骨钙素(oc,骨形成参数)和降低血清c末端腹膜(ctx)(p <.01)和蜕膜(pth)(p <.05)(骨吸收参数均。它还改变了股骨的微观结构。总之,HFD干扰了正常的骨稳态,导致骨质损失增加。在肥胖的小鼠中,B.PseudocateNulatum通过降低骨吸收和增加骨形成,CECT 7765降低骨质损失和增强的BMD。

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