Obesity is a growing public health problem worldwide, with more than one billion overweight and 300 million obese according to the WHO. Obesity contributes to serious diseases such as diabetes and cardiovascular disease. In recent years, a number of reports have shown that people who spend much of their day sitting are at increased risk of obesity and diabetes. The reasons for this association are unknown. We have now obtained results suggesting that increased sitting may lead to less activation of a "body weight sensor" in the weight-bearing long bones and that this in turn leads to reduced activity in an anti-obesity system. There is already a well-known system that aims to keep body fat mass constant. The anti-obesity hormone leptin is released into the bloodstream from adipose tissue in proportion to the size of the fat mass. Leptin exerts a negative feedback loop in the brain leading to reduced appetite and obesity. Unfortunately, for unknown reasons, most obese people are insensitive to leptin's anti-obesity effect. Our clear preliminary data show that inserting weights into the abdominal cavity of mice reduces their food intake, body weight and fat mass in relation to the size of the weight and that this effect involves a specific cell type in the long tubular bones. We now want to study the exact mechanism of how the "body weight meter" affects fat mass and the possible clinical significance of this novel system of fat regulation.