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The arthritis and joint pains that affect obese people may not be due to overworked joints, as is often assumed. Instead, the real cause of joint overload associated with obesity can be inflammation – a scale-wide inflammation caused by microbes that grow in the bowels of obese people .
An even more fundamental cause may be an imbalanced diet, so high in fat that it unbalances the intestinal microbiome. However, the joint-degrading effects of a high-fat diet can be mitigated if a prebiotic supplement is consumed.
The inflammatory link between the gut microbiome and osteoarthritis associated with obesity has been clarified by scientists based at the University of Rochester Medical Center (URMC). These scientists found that obese mice had more harmful bacteria in the intestines than lean mice, which caused inflammation throughout their body, resulting in very rapid deterioration of the joints. Although a common prebiotic supplement did not help the mice lose weight, it completely reversed the other symptoms, making the viscera and joints of obese mice indistinguishable from lean mice.
The detailed results were published on 19 April JCI Insight, in an article entitled "Targeting the intestinal microbiome to treat osteoarthritis of obesity". This article says that oligofructose, a non-digestible prebiotic fiber, can restore the profile of a lean intestinal microbial community in the context of obesity. In addition, the article demonstrates that prebiotics could be a way to treat osteoarthritis of obesity.
"Compared to the lean murine gut, obesity is associated with a loss of bifidobacteria, while key pro-inflammatory species are gaining in abundance, "wrote the authors of the article. "A downstream systemic inflammatory signature ends with a migration of macrophages to the synovium and an acceleration of osteoarthritis of the knee. Oligofructose supplementation restores the lean intestinal microbiome in obese mice, in part by supporting the commensal microflora, particularly Bifidobacterium pseudolongum. This is associated with reduced inflammation of the colon, circulation and knee and protection against osteoarthritis. "
The URMC team, led by Michael Zuscik, Ph.D., essentially fed mice with a high-fat diet similar to a Western diet called cheeseburger and milkshake. After only 12 weeks of high-fat diet, experimental mice became obese and diabetic, almost doubling their body fat percentage compared to control mice, which were fed a healthy, low-fat diet. Colonies of obese mice were dominated by pro-inflammatory bacteria and almost completely missed bifidobacteria, the beneficial probiotic bacteria.
Changes in intestinal microbiomes of mice coincided with signs of inflammation at the body level, including at the knee, where the researchers caused osteoarthritis with a meniscal tear, a common sports injury. known to cause osteoarthritis. Compared with lean mice, osteoarthritis progressed much more rapidly in obese mice, with almost all their cartilage disappearing within 12 weeks of injury.
"Cartilage is both a cushion and a lubricant, promoting frictionless joint movement," said Dr. Zuscik. "When you lose that, it's bone to bone, rock on rock. That's the end of the line, and you have to replace all the gasket. "
Surprisingly, the effects of obesity on intestinal bacteria, inflammation, and osteoarthritis were completely avoided when the high-fat diet of obese mice was supplemented with prebiotics. Prebiotics can not be digested by rodents or humans, but they are welcome for certain types of beneficial intestinal bacteria, such as bifidobacteria. Colonies of these bacteria have declined and grown, invading obese mice and crowding out bad actors, such as pro-inflammatory bacteria. This, in turn, decreased systemic inflammation and slowed cartilage degradation in the osteoarthritic knees of the mouse.
The oligofructose even made the obese mice less diabetic, but there was one thing that the dietary supplement did not change: body weight.
Obese mice given oligofructose remained obese, carrying the same burden on their joints, but their joints were healthier. Simply reducing the inflammation was enough to protect cartilage joints against degeneration, reinforcing the idea that inflammation – not biomechanical forces – resulted in osteoarthritis and joint degeneration .
"The in-depth study of the tradeoffs between microbial abundance in the context of obesity and under the influence of oligofructose is warranted," the authors of the article said. "The particular focus put on the possible influence of metabolic signatures and transcriptomics of dominant species likely to have an impact on the functioning of the host immune system and on physiology in a way that has not yet been understood is an important future direction. "
Although there are parallels between mouse microbiomes and human microbiomes, the bacteria that protected mice from osteoarthritis-related obesity may differ from bacteria that could help humans. URMC scientists want to collaborate with researchers from the military and veteran microbiome: Consortium for Research and Education within the US Department of Veterans Affairs to advance this research on humans.
The team hopes to compare veterans with OA to those who do not, to better understand the links between intestinal microbes and joint health. They also hope to test whether prebiotic or probiotic supplements that shape the gut microbiome can have similar effects in veterinarians with osteoarthritis as in mice.
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