Researchers in the US investigating the effect of the nerve messenger and mood regulator serotonin on the energy metabolism of worms, found that being obese or thin may not just be a result of one's eating habits.
The discovery was the work of Dr Kaveh Ashrafi, of the Department of Physiology and UCSF Diabetes Center at the University of California, San Francisco (UCSF), and colleagues, and is published in the 4th June issue of Cell Metabolism.
Scientists already knew that serotonin played a role in fat loss in both in the worm C. elegans and in mammals, with high levels of the brain chemical leading to fat loss and low levels leading to fat accumulation. However, there are differences, for example when serotonin is high, they may both lose fat, but in the case of the worms they also eat more, and in the case of humans, they eat less.
In this experiment the researchers think they found the answer to this difference in that serotonin acts in two independent molecular pathways: one controls fat levels and the other controls feeding behaviour. They wrote that:
"Serotonergic feeding regulation is mediated by receptors whose functions are not required for fat regulation."
Ashrafi, who is Jack and DeLoris Lange Assistant Professor of Systems Physiology at UCSF, and colleagues discovered that fat regulation depends on a neuron channel working with a G protein-coupled receptor that starts a signal cascade that encourages the breakdown of lipids (fat molecules) at peripheral sites of fat storage. The breakdown of the lipids creates intermediate chemicals in the periphery that affects feeding behaviour.
Ashrafi explained that:
"It says that the nervous system is a key regulator coordinating all energy-related processes through distinct molecular pathways."
"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," said Ashrafi.
C elegans worms directly match their feeding rates to the availability of nutrients around them; when resources are low, they build up fat reserves, and when they are plentiful, they shed them. Thus, their perception of food availability controls their metabolic state, with conservation of energy being the predominant state during scarcity so that nutrients are directed to fat storage.
However, although worms and humans differ in their response to high and low serotonin, Ashrafi and colleagues speculated "that human counterparts of feeding-independent fat regulatory genes identified in our study may similarly regulate energy balance".
Speculating on the clinical implications of their findings, if the results on C elegans can be extrapolated to humans, it could lead to therapies that manipulate fat metabolism independently of what a person eats, said the researchers.
At the moment, therapies focus on feeding behaviour, which is important, but "it's only part of the story", explained Ashrafi:
"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," he said.
News Source http://www.medicalnewstoday.com
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