Far from being inert and unchanging, a mere scaffolding to which the body's muscles and organs attach themselves, bones change constantly. Old bone cells die. New ones are born. But that's not all. According to an exciting new discovery, bones play a role in regulating blood sugar levels and fat deposits.

How is this possible? Bones act like a kind of endocrine organ, releasing osteocalcin, a hormone that influences bone formation. This hormone also increases both insulin production and the body's insulin sensitivity. It also reduces fat stores. Basically, osteocalcin levels in the bones are linked to blood sugar and body fat levels, and there is some sort of interaction back and forth.

It's a surprising finding for the uninitiated. However, some scientists are saying it makes sense when you think about it. Says Ronald Kahn, director of Harvard's Joslin Diabetes Center, "Obviously there does need to be some coordination between skeletal growth and body mass. If you carry around extra weight, your bones need to hold up under the extra pressure, so it's not surprising that your bones have a sense of body fat."

According to research conducted by Ohio State University, conjugated linoleic acid (CLA) may help reduce body fat, but it also increases your risk for nonalcoholic fatty liver disease.

In 2003, a study showed that a 2 month supplementation of CLA lowered body mass and blood sugars in diabetics. The recent studies conducted on mice fed a CLA supplemented diet lost weight very fast, but also accumulated excessive amounts of fat in their livers - a side effect of rapid weight loss. In addition, excessive accumulation of fat in the liver is associated with insulin resistance, a factor exacerbating type 2 diabetes.

Although the recent findings were conducted on mice, CLA may or may not have a similar effect on humans. CLA has been a hot selling item in supplement stores for years. I wonder what the results would be if people who have taken CLA (the t10c12 variety) for years were to discontinue use for 4 weeks. I would be curious to see the baseline and follow-up tests for body mass, insulin sensitivity and fat accumulation in the liver. Any med students out there interested in setting-up a lab profiling hepatic function in CLA poppers?

Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.

SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.

This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.