Body Fat

Just like heavy loads can cause your car’s tires to wear faster, carrying too much weight on your frame can wear your cartilage faster, particularly if your joints are out of alignment. But research in recent years has revealed the obesity/OA connection goes beyond the stress additional weight places on joints. Researchers now know that fat tissue releases inflammatory chemicals that affect the joints.

One key suspect is leptin, a hormone produced by fat cells that plays a key role in regulating appetite, says Farshid Guilak, PhD, director of orthopaedic research at Duke University. Scientists have found higher levels of leptin in samples of diseased joint cartilage compared with healthy cartilage. Furthermore, leptin levels in the joint correspond with the level of damage.  Several studies have also found that leptin levels correlated with pain levels reported by patients with OA.

To better understand the role of leptin in OA, Guilak and his colleagues studied mice engineered to lack either leptin or leptin receptors on cells. “Leptin circulates through the body, but acts in the brain to control appetite,” says Guilak, whose study was funded by the Arthritis Foundation. “To control appetite it has to bind to leptin receptors on a cell – it has to dock.” Without leptin or its receptors, the mice grew to four times the normal weight of mice, but surprisingly they did not develop osteoarthritis.

Further research by the team showed that normal mice fed a high-fat diet weighed far less than leptin-deficient mice, but did develop arthritis. “This leads us to think it may be something about the leptin molecule itself that is causing osteoarthritis,” says Guilak. “Leptin, even though it controls appetite, may actually have inflammatory effects.”

Another explanation is a high-fat diet – rather than the weight gain it tends to cause – is responsible. “If we feed mice the diet that has saturated fats and lard in it, the fatty acids themselves can be inflammatory.”