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Posted on Apr 20, 2005, 4 p.m.
By Bill Freeman
If you're having trouble eating healthy, maybe you need to speak with your internal nutritionist. Mammals including humans appear to have such a nutritionist in the form of an ancient brain molecule that regulates food choices. The enzyme and its molecular mechanism are likely to be important for all mammals that eat a varied diet comprising meat and vegetables, say researchers.
If you're having trouble eating healthy, maybe you need to speak with your internal nutritionist.
Mammals including humans appear to have such a nutritionist in the form of an ancient brain molecule that regulates food choices.
The enzyme and its molecular mechanism are likely to be important for all mammals that eat a varied diet comprising meat and vegetables, say researchers.
Called GCN2 kinase, the enzyme initiates events relaying information to the brain about foods' amino acid content.
This enables animals to adjust their food intake in favor of a more balanced meal.
Researchers have previously identified the molecular mechanism in yeast and rats. David Ron of the New York University School of Medicine and colleagues have now found it in mice, suggesting that it's likely to be conserved in humans.
"This ancient pathway in mice recognizes drops in blood amino acid levels that occur following consumption of food with an imbalanced composition," says Ron. "That recognition culminates in a behavioral response that limits consumption of the imbalanced food and favors, by default, a more balanced diet."
Balanced diet
While most of the 20 amino acids can be synthesized by the body, eight must be obtained from food.
Omnivorous animals such as humans are known to consume less of a meal lacking essential amino acids than meals that are nutritionally complete.
To determine the role of GCN2 kinase in such behavior, Ron and colleagues inactivated the enzyme in the brains of mice.
The mice subsequently had no aversion to imbalanced meals.
"There's no reason to believe that the same mechanism isn't at work in humans," says Ron.
But cultural influences and an instinctive drive to consume calorie-dense foods, says Ron, might override the molecular nutritionist's ability to promote a balanced diet.
The research is reported in the journal Cell Metabolism (read abstract).
Mammals including humans appear to have such a nutritionist in the form of an ancient brain molecule that regulates food choices.
The enzyme and its molecular mechanism are likely to be important for all mammals that eat a varied diet comprising meat and vegetables, say researchers.
Called GCN2 kinase, the enzyme initiates events relaying information to the brain about foods' amino acid content.
This enables animals to adjust their food intake in favor of a more balanced meal.
Researchers have previously identified the molecular mechanism in yeast and rats. David Ron of the New York University School of Medicine and colleagues have now found it in mice, suggesting that it's likely to be conserved in humans.
"This ancient pathway in mice recognizes drops in blood amino acid levels that occur following consumption of food with an imbalanced composition," says Ron. "That recognition culminates in a behavioral response that limits consumption of the imbalanced food and favors, by default, a more balanced diet."
Balanced diet
While most of the 20 amino acids can be synthesized by the body, eight must be obtained from food.
Omnivorous animals such as humans are known to consume less of a meal lacking essential amino acids than meals that are nutritionally complete.
To determine the role of GCN2 kinase in such behavior, Ron and colleagues inactivated the enzyme in the brains of mice.
The mice subsequently had no aversion to imbalanced meals.
"There's no reason to believe that the same mechanism isn't at work in humans," says Ron.
But cultural influences and an instinctive drive to consume calorie-dense foods, says Ron, might override the molecular nutritionist's ability to promote a balanced diet.
The research is reported in the journal Cell Metabolism (read abstract).
