Abstract
Sarcopenia represents a major health burden in industrialized country by reducing substantially the quality of life. Indeed, it is characterized by a progressive and generalized loss of muscle mass and function, leading to an increased risk of adverse outcomes and hospitalizations. Several factors are involved in the pathogenesis of sarcopenia, such as aging, inflammation, mitochondrial dysfunction, and insulin resistance. Recently, it has been reported that more than one third of inflammatory bowel disease (IBD) patients suffered from sarcopenia. Notably, the role of gut microbiota (GM) in developing muscle failure in IBD patient is a matter of increasing interest. It has been hypothesized that gut dysbiosis, that typically characterizes IBD, might alter the immune response and host metabolism, promoting a low-grade inflammation status able to up-regulate several molecular pathways related to sarcopenia. Therefore, we aim to describe the basis of IBD-related sarcopenia and provide the rationale for new potential therapeutic targets that may regulate the gut-muscle axis in IBD patients.
Highlights
The European Working Group on Sarcopenia in Older People defined sarcopenia as a progressive and generalized skeletal muscle disorder, characterized by loss of muscle mass and function, low muscle strength and poor physical performance [1]
Biologic therapy, including anti-TNF alpha agents and newer anti-interleukin, anti-integrin, and Janus kinasi (JAK) inhibitors agents used for treatment of inflammatory bowel disease (IBD), might reduce sarcopenia, blocking the catabolic effects on skeletal muscle tissue [54]
It could be hypothesized that gut microbiota (GM) targeted treatment or complementary therapy such as physical activity and nutritional supplementation could be proposed to patients suffering from IBD and sarcopenia
Summary
The European Working Group on Sarcopenia in Older People defined sarcopenia as a progressive and generalized skeletal muscle disorder, characterized by loss of muscle mass and function, low muscle strength and poor physical performance [1]. A transcriptional upregulation of Murf-1, and consequent myofibril degradation was observed in mice affected by DSS-induced colitis These latter differ from controls for the loss of skeletal muscle mass and decrease in muscle function, assessed by the significant reduction of the number of gastrocnemius myofibrils and the physical performance on rotarod test [107]. These highlight the key role of NF-kB signaling pathway in development of muscle impairment [113] It was observed an improvement of BMI and muscle parameters, described as fat free mass index, after 3 months of infliximab or adalimumab, suggesting the beneficial effect of the anti-TNF alpha therapy on the nutritional status and body composition of IBD patients [114] (Table 1). A clinical application of the TABLE 1 | Principal human studies that explored the relationship between inflammatory bowel diseases and sarcopenia
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