Fat does more than hang around inconvenient places and make it tough to pull on your favorite pair of jeans. Excess body fat can destroy joints in ways that have come to surprise researchers.

“We know that obesity is the number-one preventable risk factor for osteoarthritis but it hasn’t been studied much because everyone dismissed it as overloading joints,” says Farish Guilak PhD, a professor of orthopedic surgery at Duke University Medical Center at Durham, N.C.

He and others began to wonder whether obesity alone told the whole story of joint destruction. Some athletic endeavors put greater biomechanical forces on knees than obesity. And, people who are obese are more likely to have osteoarthritis (OA) in their wrists, fingers and hands. Our hands sometimes bear loads (think of carrying a heavy flower pot) but not our body weight (we don’t walk on our hands).

For folks so overweight as to be deemed obese (defined as twenty pounds heavier than your upper weight range), those excess pounds of fat carry hidden dangers that researchers like Guilak are just beginning to understand.

Fat, or adipose tissue in medical lingo, is home to millions upon millions of busy adipocytes, or fat cells. A flurry of research over the past few years is starting to explain how adipocytes work against the body to destroy joints by misguided responses to high levels of glucose and exposure to cytokines (immune proteins). In reaction to such exposure, adipocytes churn out high levels of their own immune proteins called adipokines.

Year after year of obesity fuels a steady barrage of friendly fire that in turn generates low-level chronic inflammation. Not an inflamed immune system, like an infection but a soft drum-beat of immune proteins that over time can damage tissues such as joints,  “that’s insidious because it’s continuous,” says Robert Mooney, PhD, professor of pathology and laboratory medicine at the University of Rochester in New York.

Mooney recently redirected his research efforts from diabetes and obesity in the liver to the effects of obesity and diabetes on musculoskeletal disease. His experience researching metabolic disturbances in diabetes told him that adipocytes could also be a bad influence on joints.

To study the link between a disrupted metabolic system and osteoarthritis, Mooney turned to a trusted mouse model of diabetic mice. In work recently published in Arthritis Research and Therapy, Mooney’s team studied whether a high-fat diet in diabetic mice would damage joints.

One group of mice ate a high-fat diet and then had surgery that mimics knee injuries in people and is designed to quickly bring on osteoarthritis. The second group of mice ate regular mouse chow until they had the surgery, and then ate the high-fat diet after surgery. At monthly intervals, the team examined bone and cartilage tissues in the knee joints for markers that would reveal signs of osteoarthritis.