— -- Your nerves, rather than your eating habits, may have a more direct role in whether you are fat or thin, according to new research.
A study on worms shows that serotonin levels in the nervous system influence feeding and fat. Serotonin, a neurotransmitter, also acts independently to control eating and what your body does with those calories once they've been consumed, the study said.
"It says that the nervous system is a key regulator coordinating all energy-related processes through distinct molecular pathways," Kaveh Ashrafi, of the University of California, San Francisco, said in a prepared statement. "The nervous system makes a decision about its state leading to effects on behavior, reproduction, growth and metabolism. These outputs are related, but they are not consequences of each other. It's not that feeding isn't important, but the neural control of fat is distinct from feeding."
Ashrafi said that given serotonin's ancient evolutionary origins, you can apply what's learned from the worms to humans.
"From a clinical perspective, this may mean you could develop therapeutic strategies to manipulate fat metabolism independently of what you eat," he said. "Now, the focus is primarily on feeding behavior. As important as that is, it's only part of the story. If the logic of the system is conserved across species, a strategy that focuses solely on behavior can only go so far. It may be one reason diets fail."
The findings were published in the June issue of Cell Metabolism.
At its most basic level, fat regulation is the balance between energy intake and expenditure; however, Ashrafi said the physiology is very complicated.
In the worms, serotonin affected feeding by involving nerve receptors not normally required for fat control. The byproducts of the signaling process ended up affecting the control of feeding behavior, Ashrafi said.
In the worms and in mammals, high serotonin levels are associated with fat reduction, while low serotonin levels lead to fat accumulation, the researchers noted. However, in the worms, when serotonin goes up, the worms desire to eat increases even as fat melts away. But in humans, high serotonin leads people to eat less and shed fat.
Serotonin's effects on fat and eating habits in the worms fit the nerve messenger's role as a sensory gauge of nutrient availability, the researchers said. When resources are scarce, worms build up their fat reserves and switch metabolic gears to save energy and direct nutrients to fat stores.
Ashrafi said serotonin's role in balancing energy across species leads him to believe that "human counterparts of feeding-independent fat regulatory genes identified in our study may similarly regulate energy balance."
Human stem cell transplant helps brain-impaired mice
Mice with a congenital brain disorder improved after receiving human neural stem cell transplants, a U.S. study finds.
The mice lacked myelin, a substance that plays a critical role in the transmission of electrical signals between nerve cells. When myelin is missing or damaged, electrical signals aren't properly transmitted. These "shiverer" mice typically die within months of birth.
Demyelination also occurs in people with multiple sclerosis.
Previous research has examined the use of cell transplantation for restoring absent or lost myelin to diseased nerve fibers. But, until now, no transplantation of human neural stem cells or of their derivatives (glial progenitor cells) had been successful in test animals.
In this new study, researchers from the University of Rochester Medical Center and a number of other universities (Cornell, UCLA and Baylor) created a new method for harvesting and purification of human fetal glial progenitor cells.
They also developed a new cell delivery strategy that uses multiple injection sites to encourage widespread and dense take-up of the transplanted cells through the central nervous system.
When the researchers used these new approaches, the transplanted cells took hold throughout the brain and spinal cord, and the mice showed robust, efficient and functional myelination. Some of the mice showed neurological improvement and a fraction of them were save by the procedure.
"The neurological recovery and survival of the mice receiving transplants was in sharp contrast to the fate of their untreated controls, which uniformly died by five months," researcher Dr. Steve Goldman, of the departments of neurology and neurosurgery at the University of Rochester Medical Center, said in a prepared statement.
"To our knowledge, these data represent the first outright rescue of a congenital hypomyelinating disorder by means of stem or progenitor cell transplantation," Goldman said. "Although much work needs to be done to maximize the number of individuals that respond to transplantation, I think that these findings hold great promise for the potential of stem cell-based treatment in a wide range of hereditary and ischemic myelin disorders in both children and adults."
The study was published in the June issue of Cell Stem Cell.
By Robert Preidt, Gannett News Service