There has been plenty of recent research focusing on how your gut bacteria can send messages to your brain controlling appetite and feelings of satiation, but a recent discovery by researchers from the Columbia University Medical Centre has revealed a previously unknown appetite-regulating mechanism that is secreted by bone cells.

The CUMC team has been researching the function of bones for many years and back in 2007 made a major discovery. They revealed that our skeletonsfunction as an endocrine organ with bone cells releasing hormones that are known to be crucial in regulating energy metabolism.

The team’s initial studies discovered that bone cells release a hormone called osteocalcin, which controls the regulation of blood sugar. After disabling a certain gene in the bone-forming cells (osteoblasts) of mice, it was noted that the animal’s appetite significantly dropped.

“Since osteocalcin does not regulate appetite, we knew that a second bone hormone had to be involved in this process,” explains associate professor Stavroula Kousteni, who led the study.

This mysterious second hormone was recently revealed as being lipocalin 2, a protein known to contribute to obesity and previously linked to activating neurons in the brain related to appetite suppression. Until now it was thought that lipocalin 2 was mainly secreted by fat cells (adipocytes) but the CUMC research found levels of the hormone to be ten times higher in osteoblasts than previously found in adipocytes.

After modifying mice that lack lipocalin 2, it was found that without the hormone the animals displayed increased appetite and compromised metabolism. The team discovered that lipocalin 2 activates melanocortin 4 receptor neurons in the hypothalamus, a specific area that has been shown to be involved in triggering appetite suppression.

It appears that these bone hormones have range of systemic effects, ranging from male fertility to kidney function. “Our findings add a critical new function of bone hormones to this list—appetite suppression—which may open a wholly new approach to the treatment of metabolic disorders,” says Dr Kousteni.

It’s hoped that the discoveries around the metabolic effects of hormones released by bone cells could lead to new treatments for a variety of metabolic disorders including type 2 diabetes.

The team has already begun translating its research across into human studies, examining the blood levels of lipocalin 2 in patients with type 2 diabetes. Initial results have been positive, showing an inverse correlation between the level of the hormone and a patient’s body weight, meaning the higher the levels of lipocalin 2, the lower the body weight and better the glucose balance.