Reduced function of protein hormone, leptin, protects against development of OA with obesity
In 2005 the World Health Organization (WHO) estimated that globally 400 million adults were obese, defined by a body mass index (BMI) of 30 kg/m2 or greater. WHO projects that by 2015 there will be more than 700 million obese adults worldwide. Obesity is considered to be one of the greatest risk factors for osteoarthritis, a progressive musculoskeletal disorder that is characterized by loss of joint cartilage.
Researchers from Duke University, supported by a grant for the National Institutes of Health (NIH), studied leptin-deficient mice to determine the role of obesity in developing knee osteoarthritis (OA). Researchers believed that obesity caused by a leptin deficiency would result in a higher incidence of knee OA. Mice with a disruption of leptin signaling showed a 3-fold increase in body mass and 10-fold increase in body fat, but surprisingly did not display effects of knee OA. The findings of this study are published in the October issue of Arthritis & Rheumatism, a journal of the American College of Rheumatology.
The Duke Researchers compared leptin-deficient and leptin receptor-deficient female mice with wild-type mice to further understand the role this deficiency may play in increasing risk of knee OA. At 10-12 months of age mice were measured for body fat content and blood samples were taken to determine the level of inflammation in the animals. Knee joints were analyzed to determine bone thickness and to look for degenerative changes in the lateral femur, lateral tibia, medial femur, and medial tibia.