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."

Knocking out the gene for a peptide associated with insulin was shown to protect mice against the harmful effects of a high-fat diet. Urocortin 3 plays a role in the increased production of insulin in response to high caloric intake in animals.

Scientists found that by removing the urocortin 3 gene from mice, they did not develop the age-related insulin resistance and high blood sugar observed in the normal control mice. The metabolisms of normal mice were compared to the metabolisms of those without the urocortin 3 gene. When placed on a high caloric diet for three months, the mice without the urocortin 3 gene packed on the same amount of weight but had lower insulin levels. But these mice also had lower blood sugar, improved glucose tolerance curves and they did not develop the fatty livers the control mice experienced.

Scientists hypothesize that by curtailing the abnormally high insulin levels, they were able to manipulate insulin sensitivity and avoid some of the untoward consequences of the high food intake and weight gain. Like many of us diabetics already know too well - while insulin is effective at lowering blood sugar it also promotes fat storage. This is a natural protective response to prepare for times when food may not be available. When insulin is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organs.

Urocortin 2 and urocortin 3 are part of the system that governs the body's response to insulin. Scientists already know that mice on a high-fat diet do better if either urocortin 2 or urocortin 3 is removed. Now they want to know if the mice will respond even better if both are missing. Such results may instruct us how best to develop therapeutic means to exploit these powerful effects.

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?