Scientists believe they are closer to understanding how to control appetite.
Drug manufacturers are looking at ways to suppress appetite
Two studies in Science magazine look at brain cells, and their signals, that appear to drive weight loss and suppress hunger.
Killing off particular neurons or boosting a protein that keeps neurons alive makes mice lose weight by eating less.
The US teams from Boston and Seattle say the similar appetite pathways are present in humans.
Scientists have already been trying to develop weight-loss drugs that act on these brain pathways.
The first study in Science looked at a compound called ciliary neurotrophic factor (CNTF). This protein has been shown to cause weight loss in both humans and mice.
It is thought to work by blocking the hunger signals that stimulate appetite, but its exact action is not clear.
Dr Maia Kokoeva and colleagues at Harvard Medical School looked what happened when they gave CNTF to mice.
CNTF prompted the growth of new neurons in an area of the brain called the hypothalamus, which plays a crucial role in controlling appetite and energy balance.
They believe that CNTF has a dual action. During treatment it activates a pathway in the hypothalamus that makes the brain more responsive to the hormone leptin, which is made by fat cells and tells the body how well fed it is.
By triggering the growth of more leptin-responsive neurons, it also makes the body more sensitive to leptin even after the treatment is stopped, they told Science.
The second study, by a team at the University of Washington, looked at the neurons involved in appetite - POMC and NPY/AgRP.
POMC neurons are know to send signals to the brain to reduce appetite and mice with defects in these neurons eat excessively and become obese.
In comparison, when the researchers eliminated NPY/AgRP neurons in adult mice the animals began to eat less and less, suggesting these neurons act in opposition to POMC.
However, when they killed off the NPY/AgRP neurons in baby mice these animals continued to eat normally and maintained a normal body weight.
The findings suggest that if NPY/AgRP neurons are eliminated before they become fully functional, then animals somehow compensate.
Lead researcher Dr Richard Palmiter said: "Everybody in the field believes that NPY/AgRP neurons and POMC neurons are undoubtedly doing the same in humans as they do in rodents. So I would predict that if you could do the experiment in humans, the results would be the same."
He believes that mutations in human genes that affect the survival of these neurons or their ability to respond to hormonal signals could explain why some people are naturally very thin and others are overweight.
Dr Gavin Bewick, Dr James Gardiner and Professor Steven Bloom at Imperial College London, UK, have been looking at NYP/AgRP and were the first to demonstrate that loss of these neurons leads to reduced appetite and weight.
They said: "We are at last beginning to understand how the brain works. Together these papers suggest that switching NPY neurones off could cure obesity."