Department of Rehabilitation, Jinniu District People's Hospital of Chengdu, Chengdu, China.
Department of Orthopedics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Front Cell Infect Microbiol. 2021 Jul 14;11:636231. doi: 10.3389/fcimb.2021.636231. eCollection 2021.
Long-term and excessive alcohol consumption are risk factors for osteoporosis. Excessive drinking can reduce bone density and also cause imbalance of gut microbiota. And gut microbiota can affect bone metabolism through various mechanisms, and the regulation of gut microbiota is closely related to age. However, the effects of gut microbiota on alcohol-induced osteoporosis at different ages are unclear. In this study, young and old rats were used to induce osteoporosis by long-term alcohol consumption, and alcohol metabolism, bone morphology, bone absorption and immune activity of rats were analyzed to determine the effects of alcohol on rats of different ages. In addition, changes of gut microbiota in rats were analyzed to explore the role of gut microbiota in alcohol-induced osteoporosis in rats of different ages. The results showed the ability of alcohol metabolism was only associated with age, but not with alcohol consumption. Long-term alcohol consumption resulted in the changes of bone metabolism regulating hormones, bone loss, activation of receptor activator of NF-B ligand (RANKL) signaling and inflammatory response. And osteoporosis was more severe in old rats than young rats, suggesting that alcohol-induced osteoporosis is age-related. In addition, long-term drinking also affected the composition of gut microbiota in rats, with a significant increase in the proportion of pro-inflammatory microorganisms. Overall, this study found that long-term alcohol consumption induced osteoporosis and affected the composition of gut microbiota. And alcohol can activate T lymphocytes directly or indirectly by regulating the changes of gut microbiota to produce cytokines, and further activate osteoclasts. In addition, the osteoporosis was more severe in the old rats than young rats, which may be due to the higher diversity and stronger regulation ability of gut microbiota in young rats compared with old rats.
长期和过量饮酒是骨质疏松症的危险因素。过量饮酒会降低骨密度,还会导致肠道微生物群失衡。肠道微生物群可以通过多种机制影响骨代谢,而肠道微生物群的调节与年龄密切相关。然而,肠道微生物群对不同年龄酒精性骨质疏松的影响尚不清楚。在这项研究中,使用年轻和老年大鼠通过长期饮酒来诱导骨质疏松症,并分析大鼠的酒精代谢、骨形态、骨吸收和免疫活性,以确定酒精对不同年龄大鼠的影响。此外,还分析了大鼠肠道微生物群的变化,以探讨肠道微生物群在不同年龄大鼠酒精性骨质疏松症中的作用。结果表明,酒精代谢能力仅与年龄有关,而与饮酒量无关。长期饮酒导致调节骨代谢的激素变化、骨丢失、核因子-κB 受体激活配体(RANKL)信号的激活和炎症反应。并且老年大鼠的骨质疏松症比年轻大鼠更严重,表明酒精性骨质疏松症与年龄有关。此外,长期饮酒还影响了大鼠肠道微生物群的组成,促炎微生物的比例显著增加。总的来说,这项研究发现长期饮酒会引起骨质疏松症,并影响肠道微生物群的组成。此外,酒精可以通过调节肠道微生物群的变化直接或间接地激活 T 淋巴细胞产生细胞因子,进而激活破骨细胞。此外,老年大鼠的骨质疏松症比年轻大鼠更严重,这可能是由于年轻大鼠的肠道微生物群多样性更高,调节能力更强。