A new study offers insight as to why keeping up with exercises and other physical activities could be so difficult. The study links a deficit in dopamine to the reduced physical activity in mice.
The study’s lead researcher Alexxai Kravitz from the Diabetes, Endocrinology, and Obesity Branch of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), wondered why obese animals have a hard time in carrying out normal physical activity.
It is a common perception that animals or persons that are obese are mostly physically inactive because they have to carry more body weight. However, Kravitz noticed similarities between obese mice and Parkinsonian mice during his study. He thought that perhaps another factor contribute to the physical inactivity, according to MNT.
He hypothesized that a dysfunction in rodents’ dopamine system might provide a possible explanation of their lack of physical activity.
“Other studies have linked dopamine signaling defects to obesity, but most of them have looked at reward processing – how animals feel when they eat different foods. We looked at something simpler: dopamine is critical for movement, and obesity is associated with a lack of movement,” he added.
The researchers examined dopamine signaling in both lean and obese mice. They fed a group of mice with a normal diet and another group with a high-fat diet for 18 weeks.
After 2 weeks, the mice on a high-fat diet gained more weight than the lean ones. By week 4, the obese mice spent less time moving and were slower when they did move compared to the lean mice.
The researchers examined whether there is a relationship between the changes in movement and the weight gain, but found no correlation. Amazingly, the mice on a high-fat diet moved less even before they gained most of the weight, which invariably suggests that the extra weight could not have been responsible for the reduced movement, according World Times 24.
To identify the mechanisms behind the less physical activity, Kravitz and team quantified several aspects of dopamine signaling and found that the D-2 type receptor (D2R) binding, found in the striatum, was reduced in obese mice. This was consistent with previous research in rodents.
They genetically removed the D2Rs from the striatum of lean mice to check whether there was a causal link between the D2Rs and the reduced activity and then placed the lean mice on a high-fat diet. They discovered that the mice did not gain more weight, despite their physical inactivity.
This finding suggests that although deficits in striatal D2R contribute to physical inactivity in obesity, the reduced activity is more a consequence than a cause of obesity, according to the study authors.
There are probably other factors involved as well, the deficit in D2 is sufficient to explain the lack of activity, first author of the study, Danielle Friend says.
Kravitz noted that his future research will examine the connection between diet and dopamine signaling. He and his team will investigate whether unhealthy eating affects dopamine signaling, and how quickly mice recover to their normal activity levels once they start eating healthy and losing weight.
He hopes that his research will help to relieve some of the stigma faced by people with obesity. The researchers published their findings in the journal Cell Metabolism.
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