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Brain Rewards Obesity

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Brain Rewards Obesity

By Rick Nauert, Ph.D.

      Senior News Editor

      Reviewed by John M. Grohol, Psy.D. on July 30, 2008

 

Wednesday, Jul 30 (Psych Central) -- A new study of food reward and addictive

behaviors finds that the tendency toward obesity is directly related to a

response from the brain.

 

 

 

Researchers at Tufts University School of Medicine (TUSM) and colleagues have

demonstrated a link between a predisposition to obesity and defective dopamine

signaling in the mesolimbic system in rats.

 

Their report appears in the August 2008 issue of The FASEB Journal.

The mesolimbic system is a system of neurons in the brain that secretes

dopamine, a neurotransmitter or chemical messenger, which mediates emotion and

pleasure. The release of the neurotransmitter dopamine in the mesolimbic system

is traditionally associated with euphoria and considered to be the major

neurochemical signature of drug addiction.

 

“Baseline dopamine levels were 50 percent lower and stimulated dopamine release

was significantly attenuated in the brain reward systems of obesity-prone rats,

compared with obesity-resistant rats. Defects in brain dopamine synthesis and

release were evident in rats immediately after birth,” said Emmanuel Pothos,

PhD, assistant professor in the department of pharmacology and experimental

therapeutics at TUSM.

 

“Previous research has demonstrated that food intake leads to an increase in the

release of dopamine, in the circuits that mediate the pleasurable aspects of

eating,” Pothos explains.

 

“Also, chronic food deprivation resulting in decreased body weight leads to

decreased dopamine levels. Therefore, increased food intake may represent a

compensatory attempt to restore baseline dopamine levels.”

Pothos says, “These findings have important implications in our understanding of

the obesity epidemic. The notion that decreased dopamine signaling leads to

increased feeding is compatible with the finding from human studies that obese

individuals have reduced central dopamine receptors.”

 

He speculates that an attenuated dopamine signal may interfere with satiation,

leading to overeating.

 

Pothos and colleagues conducted their research using obesity-prone and

obesity-resistant rats. Adult obesity-prone rats consumed more food and were 20

percent heavier than obesity-resistant rats.

 

The researchers measured electrically-evoked dopamine release from nerve

terminals. “We also measured regulators of dopamine synthesis and release in

midbrain dopamine pathways,” explains Brenda Geiger, first author and graduate

student in the pharmacology and experimental therapeutics department at TUSM.

 

“Our molecular analysis suggests that the central dopamine deficits are most

likely caused by reduced expression of the genes encoding two proteins, one that

is involved in dopamine synthesis, and another that is a transporter responsible

for packaging dopamine into vesicles from which it is later released upon

stimulation.”

 

“Obesity has so far been approached mostly as a metabolic rather than as an

addictive disorder; and obesity research has primarily focused on brain systems

that regulate body weight through the maintenance of energy balance.

 

The current study challenges this approach by focusing on brain pathways

implicated in pleasure and reward. These pathways could override energy balance

and induce hyperphagia and obesity by altering the reward value of food,

particularly palatable high-energy food, very early in life,” says Pothos, who

is the study’s corresponding and senior author.

 

According to Gerald Weissmann, MD, editor-in-chief of The FASEB Journal, “Now we

know why so many people stay addicted to food: it fuels the mid-brain pleasure

machinery. We eat not only for nourishment, but also for pleasure. This study

provides the molecular link between eating and mental health.”

 

Source: Tufts University, Health Sciences

 

http://psychcentral.com/news/2008/07/30/brain-rewards-obesity/2669.html

 

 

 

 

 

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