Pupil constriction during sleep may protect the murine brain from being awakened by sudden flashes of light.
A study links excess body weight in the rodents with dopamine receptor inactivity and reduced movement.
January 3, 2017|
WIKIMEDIA, SUNHOLMExperiments in mice find that obesity reinforces a sedentary lifestyle. According to a December 29 study in Cell, obese mice were less active due to changes in their dopamine receptors—specifically, a drop in activity in DR2 receptors in the brain’s striatum, which plays a role in motor control.
“There’s a common belief that obese animals don’t move as much because carrying extra body weight is physically disabling,” coauthor Alexxai Kravitz of the National Institute of Diabetes and Digestive and Kidney Diseases said in a press release. “But our findings suggest that assumption doesn't explain the whole story.”
Kravitz and colleagues fed mice either a standard diet or a high-fat diet for 18 weeks, and then examined their dopamine signaling pathways. They found that the least active mice had less-active DR2 dopamine receptors in the striatum. Then they genetically engineered mice to have the same DR2 deficiency, and found that even those that remained lean engaged in less physical activity than other mice. Together, the findings suggest that the DR2 deficiency may account for a lack of movement in obese mice.
“Other studies have connected dopamine signaling defects to obesity, but most of them have looked at reward processing—how animals feel when they eat different foods,” Kravitz said in the press release. “We looked at something simpler: dopamine is critical for movement, and obesity is associated with a lack of movement. Can problems with dopamine signaling alone explain the inactivity?”
This does not necessarily prove that obesity impairs the DR2 receptor. As STAT reported, it is also possible that the high-fat diet may have given rise to the DR2 deficiency. “So they feed the mice this high-fat diet, it impairs the receptor, and that decreases activity,” Vicki Vieira-Potter, a University of Missouri physiologist who was not involved in the study, told STAT. “To call inactivity a consequence and not a cause of obesity is a broad misreading of what their research shows.”