Eating and weight regulated by neurons
14/09/2005 - Fundamental research reveals two parts of a neuronal system, one that promotes eating and another that suppresses eating, are critical for the acute regulation of eating and body weight.
Researchers at Yale School of Medicine highlight that the agouti-related peptide-expressing (AgRP) neurons are mandatory for eating.
"Previous studies showed that the brain, particularly the hypothalamus, is responsible for the regulation of eating," said co-senior author Tamas Horvath.
"But until now, no experimental evidence was available to prove that AgRP neurons are critical for acute regulation of eating," he adds.
The scientists claim their research can aid the multibillion academic approach against metabolic disorders, on the fringe of which lies a slice of food research.
Food developers are focusing efforts on formulations to crack the obesity phenomenon, currently gaining momentum across the world.
Fresh figures released show in excess of 200 million adults across the EU may be overweight or obese.
And the number of European kids overweight is rising by a hefty 400,000 a year, according to the data from the International Obesity Task Force (IOFT).
Obesity is associated with metabolic and cardiovascular disorders often referred to as the metabolic syndrome, which increases an individual's risk of developing a serious disease.
Horvath's collaborator Jens Bruening at the University of Cologne in Germany introduced the avian diphtheria toxin receptor into neurons in the feeding support system of transgenic mice.
When the animals were adults, two injections of toxin caused the specific cell population to die within 48 hours, impairing the mouse's ability to eat and resulting in acute anorexia. These mice also showed marked reduction in blood glucose, plasma insulin and leptin ? the ?reg;appetite' hormone - concentrations.
"Our results confirm the hypothesis that these two systems are critical for eating and the cessation of eating," said Horvath, adding that previous transgenic approaches failed to provide this proof because of compensatory mechanisms that could operate during development.
But none of those actually knocked out neuronal function. "In this case, however, neurons are gone and there is no time to replace their function," he says.
Full findings for the study are published in Nature Neuroscience, 11 September, October 2005 Vol. 8 No. 10 .
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