Abstract
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-κB 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.
Highlights
Osteoporosis (OP) is a skeletal disorder characterized by reduced bone mass, altered bone microstructure, increased bone fragility and fracture risk (Lamichhane, 2005)
The results showed that the levels of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) in the old rats were significantly lower than that of the young rats both in the control and alcohol group (P < 0.05), suggesting that the ethanol metabolism ability of the old rats was weaker than that of the young rats
The alcohol intake had no significant effects on the enzyme activity of ethanol metabolism in the old or young rats (Table 1)
Summary
Osteoporosis (OP) is a skeletal disorder characterized by reduced bone mass, altered bone microstructure, increased bone fragility and fracture risk (Lamichhane, 2005). The incidence of osteonecrosis, osteoporosis, and fractures caused by alcohol abuse and alcohol dependence is gradually increasing (Maurel et al, 2012). Alcohol-induced osteoporosis (AOP) is a disorder of systemic bone metabolism, which belongs to secondary OP (Abukhadir et al, 2013) and is very common in clinical practice. With the increase of age, the rate of bone turnover increases at the tissue level, leading to damaged osteoblast bone formation and increased osteoclast bone resorption, significantly increasing the incidence of osteoporosis (Khosla and Riggs, 2005; Manolagas and Parfitt, 2010)
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