12 January - 20 June 2016

Fat in the bones: the effect of diet and exercise

02 July 14

The composition of bone is complex and dynamic. Its marrow produces blood, immune cells, and fat in proportions that change with age and, as recent research shows, in accordance with other factors such as diet and exercise. A paper just published in Bone considers the particular impact of fat in the bone, and its conclusions may increase our understanding of bone fracture in the elderly.

In the bone marrow, a particular type of stem cell (mesenchymal cell) is known to produce new bone. As we age, however, the mesenchymals start to produce fat cells instead. This phenomenon has prompted bone researchers to consider the relationship between the increase in bone fat with age and increased risk of bone fracture.

A team led by Maya Styner of the North Carolina School of Medicine studied the factors affecting bone fat by observing how levels varied between mice fed a normal diet, and mice fed a high fat diet. They combined this with investigation of the effect of exercise. The researchers found that when mice on a normal diet could run on a wheel as much as they wanted, their bone fat content substantially decreased compared to the control group of sedentary mice.

When the mice were fed a high fat diet, the bone fat of the sedentary group shot up 2.6-fold over ten weeks. However, when the obese mice were allowed to exercise as much they wanted whilst continuing this high fat diet, their bone fat decreased significantly, and in fact to a similar level to that observed in the sedentary mice fed a normal diet.

In another experiment discussed by Styner, mice were fed with rosiglitazone, a diabetes drug which is known to lower blood sugar, but increase marrow fat. Taking the drug increased the mice's risk of bone fracture, but when they were allowed to exercise, the bone-fattening effect - and, it is inferred, the fracture risk - was lessened.

This research has added to the body of evidence suggesting that exercise increases bone quality, and could therefore help protect against fracture. What we do not yet know, however, is the mechanism by which this occurs, whether the mouse results can be extrapolated to humans, and, if they can, what activity levels humans would have to reach to see similar protective effects. Nevertheless, Styner's team's work contributes to a research base that could go on to help populations at high risk for bone fracture, such as the elderly, people with diabetes and those taking steroids (which are known to be fat-inducing).

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