Couch potatoes gain weight without eating

Not just the eating but also the actual position of “couch potatoes” is harmful, new research shows.

By JUDY SIEGEL-ITZKOVICH
couch potato 311 (photo credit: Thinkstock/Imagebank)
couch potato 311
(photo credit: Thinkstock/Imagebank)
It has been known for some time that people who watch hours of TV a day tend to be at higher risk of becoming overweight or obese. The connection was thought to be because of munching junk food while watching. But Tel Aviv University researchers have found that not just the eating but also the actual position of “couch potatoes” is harmful.
Being stretched out in front of the TV is considered to be “active inactivity” and causes viewers to gain weight.
Such inactivity actually encourages the body to create new fat in fat cells, says Prof. Amit Gefen of the department of biomedical engineering. Along with his doctoral student, Naama Shoham, Gefen has shown that preadipocyte cells – the precursors to fat cells – turn into fat cells faster and produce even more fat when subject to prolonged periods of “mechanical stretching loads” – the kind of weight we put on our body tissues when we sit or lie down.
The research, published recently in The American Journal of Physiology – Cell Physiology, demonstrates another damaging effect of a modern, sedentary lifestyle. “Obesity is more than just an imbalance of calories,” Gefen notes. “Cells themselves are also responsive to their mechanical environment.
Fat cells produce more triglycerides, and at a faster rate, when exposed to static stretching.”
Gefen, who investigates chronic wounds that plague bedridden or wheelchair-bound patients, says that muscle atrophy is a common side effect of prolonged inactivity.
Studying MRI images of the muscle tissue of patients paralyzed by spinal cord injuries, he noticed that over time, lines of fat cells invade major muscles. This discovery led to an investigation into how mechanical load – the amount of force placed on a particular area occupied by cells – could be encouraging fat tissue to expand.
In the lab, the researchers stimulated preadipocytes with glucose or insulin to differentiate them into fat cells. Then they placed individual cells in a cellstretching device, attaching them to a flexible, elastic substrate.
The cells were stretched consistently for long periods of time, representing extended periods of sitting or lying down, while a control group of cells was not. Tracking the cultures over time, the researchers noted the development of lipid droplets in both the test and control groups of cells.
After just two weeks of consistent stretching, the test group developed significantly more – and larger – lipid droplets. By the time the cells reached maturity, the cultures that had been mechanically stretched had developed 50 percent more fat than the control culture. They were, in effect, fatter by half again.
According to Gefen, this is the first study that looks at fat cells as they develop, taking into account the impact of sustained mechanical loading on cell differentiation. “There are various ways that cells can sense mechanical loading, which helps them to measure their environment and triggers various chemical processes,” he says. “It appears that long periods of static mechanical loading and stretching, due to the weight of the body when sitting or lying, has an impact on increasing lipid production.” The evidence indicates that we need to take our cells’ mechanical environment into account and pay attention to calories consumed and burned, Gefen suggests. Although there are extreme cases, such as people confined to wheelchairs or beds due to medical conditions, many of us live too sedentary a lifestyle, spending most of the day behind a desk. Even someone with healthy diet and exercise habits will be negatively impacted by long periods of inactivity.
The researchers will now investigate how long a period of time a person can sit or lie down without the mechanical load becoming a factor in fat production. But in the meantime, it certainly can’t hurt to get up and take an occasional stroll, he suggests.
WHITE CELL ‘SELECTORS’
The white blood cells that fight disease and help our bodies heal are sent to sites of infection or injury by “exit signs” – chemical signals that tell them where to pass through the blood vessel walls and into the underlying tissue. New research at the Weizmann Institute of Science that appeared online recently in Nature Immunology shows how cells lining blood vessel walls may act as “selectors” by hiding signals where only certain “educated” white blood cells find them.
In previous studies, Prof. Ronen Alon and his team in the Rehovot institute’s immunology department had found that near sites of inflammation, white blood cells rapidly crawl along the inner lining of the blood vessels with tens of tiny “legs” that grip the surface tightly, feeling their way toward the exit sign. These signs consist of migration-promoting molecules called chemokines, which endothelial cells lining the blood vessels display on their outer surfaces like flashing lights.
In the new study, Alon and his team found that not all chemokine signals produced by endothelial cells are on display.
They observed the recruitment of subsets of immune cells called effector cells that act as the “special forces” of the immune system. They receive training in the lymph nodes, where they learn to identify a particular newly-invading pathogen and then return to the bloodstream on a search-and-destroy mission. Like the other white blood cells, effector cells crawled on tiny appendages along the lining of inflamed blood vessels near the site of pathogen entry, but rather than sensing surface chemokines, they used their legs to reach into the endothelial cells in search of the migration-promoting chemokines.
As opposed to the external exit signs, these chemokines were held in tiny vesicles inside the inflamed endothelial cell walls. The effector cells paused in the place where several cells met, inserting their legs through the walls of several endothelial cells at once to trap chemokines as they were released from vesicles at the endothelial cell membrane.
Once they obtained the right chemokine directives, the immune cells were quickly ushered out through the blood vessel walls toward their final destination.
The researchers think that keeping the chemokines inside the endothelial cells ensures that these vital signals will be safe from getting washed away in the blood or eaten by various enzymes, while at the same time guaranteeing that only those effector cells with special training to find the signals will pass through.
“We are now seeing that the blood vessel endothelium is much more than just a passive, sticky barrier; It actively selects which recruited cells actually cross the barrier and which will not,” says Alon. The endothelial cells seem to play an active role in showing the immune cells the right way out, though we’re not sure exactly how. Moreover, we think that tumors near blood vessels might exploit these trafficking rules for their benefit by putting the endothelial cells in a quiescent state or making the endothelium produce the “wrong” chemokines. Thus, immune cells capable of destroying these tumors will not be able to exit the blood and navigate to the tumor site, while other immune cells that aid in cancer growth will.”