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March 31, 2017 | 3 minute read

Bone-derived Hormone Regulates Appetite in Mice

We often think of bones as static, lifeless structures, but scientists are learning that bones are far more dynamic than once believed and play important roles in immunity, kidney health, and metabolism. Now research published in Nature has identified a hormone produced by bone cells that helps regulate appetite in mice, a finding that adds to the understanding of weight management and potentially cancer risk.

Obesity increases risk of many types of cancer.

Scientists have long known that fat cells produce a hormone called lipocalin-2, but the researchers in this study discovered that bone-forming cells produce as much as 10 times more lipocalin-2 than fat cells.

Mice who produced the hormone lipocalin-2 in fat cells only (top) ate more than mice with bone-derived lipocalin-2. Nature, March 2017

The researchers wanted to understand whether bone-derived lipocalin-2 plays a role in regulating appetite, so they bred two groups of mice: one whose fat cells couldn’t produce lipocalin-2 and one whose bone cells couldn’t produce lipocalin-2.  They compared the two groups to normal “wild type” mice.

Mice whose fat cells couldn’t produce lipocalin-2 had the same level of appetite as wild type mice. But mice whose bone cells couldn’t produce lipocalin-2 had greater appetites. In fact, the adult mice ate more than 16% more than wild type mice, and young mice ate nearly 24% more! The mice with greater appetites also had poor blood sugar control, insulin resistance, and more body fat than both the wild type mice and those whose fat cells couldn’t produce lipocalin-2, suggesting that the bone-derived lipocalin-2 alone was responsible for the changes in appetite and metabolism.

Next, the scientists investigated whether lipocalin-2 was traveling to the brain to regulate appetite. They bred another group of mice whose entire bodies couldn’t produce lipocalin-2. They injected the mice with lipocalin-2 and observed that the hormone accumulated in the brain (just like it does in wild type mice), where it bound to and activated a receptor that helps curb appetite.

The researchers noted that lipocalin-2 may alter metabolism in humans, too. They measured levels of lipocalin-2 in the blood of men with diabetes and found that lipocalin-2 levels were lower in the men who had poor blood sugar control or had higher body weight. Adults who have type 2 diabetes are at risk of developing cancer and are nearly twice as likely to develop cancers of the liver, pancreas, and endometrium.

The scientists weren’t sure why bone-derived lipocalin-2 suppressed the mice’s appetite, but they speculated that the hormone might help maintain healthy bones. During periods of low calorie intake, bone formation can slow, and lipocalin-2 levels drop. Low levels of lipocalin-2 would stimulate appetite to give your body the nutrients it needs to promote bone development. Once a healthy level of bone was achieved, the bone-forming cells would send lipocalin-2 to the brain to curb appetite.

Future research may show that our bones play even more roles in maintaining a healthy metabolism—and potentially reducing cancer risk.

Thanks to Teresa Johnson for guest blogging.

Teresa L. Johnson, MSPH, MA, RDN, is a nutrition and health communications consultant with a long-time interest in the role of plant-based diets and cancer prevention. Her work draws on elements of nutritional biochemistry, phytochemistry, toxicology, and epidemiology.

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