CABI Blog

According to a study published in Cell Metabolism, the brain circuitry of obese mice is in denial about the state of the rest of the mouse’s body. While this may also be true of the conscious brains of many overweight or obese human subjects, research hasn’t yet extended this far, except in the numerous body image studies that, unsurprisingly, have tended to show the opposite effect.

Michael Cowley’s group at Oregon Health and Science University have shown that the problem of diet-induced obesity in these mice may be due to leptin resistance, rather than a lack of leptin. Most obese humans and rodents don’t respond to leptin’s appetite-suppressing effects, which may explain the lack of success of attempts to turn it into the anti-obesity wonder drug it was once predicted to become. The group fed two groups of genetically identical adult mice the same high-fat diet for 20 weeks, but only around 60% became fat, roughly equivalent to the statistics for American adults. While leptin was found to be released in all the mice in response to high fat diets, in the ones that became obese, it failed to elicit its appetite suppressing effects, essentially because the brain didn’t recognise it was there.

The next target for investigation is the suppressing effect of SOCS-3, a protein that is believed to be responsible for leptin resistance and to repeat the mouse experiment with primates, which are a little closer to humans in their behaviour.

This finding, however, does not provide an excuse to all those of us struggling to shift the pounds. A nice surprise to the Oregon group was that decreasing the fat content of the mouse’s diet without decreasing the energy concentration restored the mice’s weight to normal.

Read more about obesity, leptin, SOCS-3 and even overweight mice, if you like, on CABDirect; nutritionandfoodsciences.org; or go straight to Michael Cowley’s research page.