Many of us make New Year's resolutions to get into better shape, maybe by joining a gym or starting running. All too often, we don't last the distance, and a mouse study might yield clues as to why.
Despite all our best intentions to lose those pounds piled on over Christmas, it doesn't always work out. All too often, exercise plans - like regularly attending the gym - go by the wayside before January is through.
In a study reported in the journal Cell Metabolism, US scientists found that diet and dopamine - one of the so-called happiness hormones - might be a factor in our motivation.
Researchers at the National Institute of Diabetes and Digestive and Kidney Diseases in Maryland were interested in why obese mice don't tend to move. They wondered whether it was the cumbersome extra weight alone that made mice prone to laziness, or if something else was also at work.
"If you look at an obese mouse, you could study a lot of different things but something that's really obvious is that it doesn't move very much, it kind of sits in the corner," lead researcher Alexxai Kravitz told DW.
Dopamine might help help explain not only why we want to eat more, but also why we want to move less
"One suggestion which certainly contributes is that, of course, if the body weighs twice as much then it's harder to move and that might be the explanation. We came to the idea that it definitely contributes but it's not the whole picture."
"Once you rule out that it's not just the size of the mouse, then you start thinking 'What else is different about this mouse and one of the larger literatures on obesity and the brain involves the dopamine system. Dopamine is an interesting molecule in that it has been implicated in a number of different brain functions."
"You can read about dopamine impacting on reward and feelings of pleasure, meaning that you would take a group of people with or without obesity and look at their response to sugar and fats and cues that predict them."
"Something that hadn't been looked at was, 'What about the role of dopamine and movement in obesity?'"
Parallels with Parkinson's
There was another reason Kravitz thought dopamine might be the key. He had a background in researching Parkinson's disease - caused by a lack of dopamine in the brain - when he started conducting studies on obesity. Kravitz was surprised by the similarities between obese mice and those with Parkinson's.
The team fed mice on either a standard or high fat diet for 18 weeks. By the fourth week, the fat-fed mice stopped moving, and moved more slowly when they did. Kravitz' team decided to examine six different parts of the dopamine system in the brain, from dopamine itself to dopamine receptors and intracellular messengers.
They found that the obese, inactive mice had far fewer D-2 receptors in an active state. Receptors act like radio antennae picking up chemical signals so that a cell - in this case nerve cells - can act on them.
Diet and behavior
It was notable early on that mice on the high fat diet didn't have to gain weight before they stopped moving - they slowed down even before fat presented a physical handicap.
More light might be shed on that in the future, with research planned into how unhealthy eating affects dopamine signaling. Future research will also look into how quickly "junk food" mice recover normal activity levels once they are fed on a healthy diet.
However, Kravitz says the most important aspect will be in understanding individual behavior.
"I have to stress that it's a mouse study, which is important when it comes to trying to draw conclusions for human health."
"I think the main thing for me is that it kind of increases our understanding of why it's so difficult to change activity levels, especially in people with obesity. I think everybody who's tried to adhere to a new gym regimen knows that it's very difficult to keep up with it."