Data Support Idea That Zinc Plays Key Role In Fight Against Anorexia

September 04, 1998

CHAMPAIGN, Ill. -- People who don't consume zinc may become seriously anorexic, with little desire and even a repulsion for eating. For many young, weight-conscious women, and often the elderly, not eating becomes a state of mind and is considered a serious psychiatric disorder.

A series of projects involving food intake and zinc deficiency at the University of Illinois are unwrapping the biological-brain mystery. In articles published in Nutritional Biochemistry (January) and the Journal of Nutrition (January, July), a team led by Neil F. Shay reports a rise in neuropeptide Y (NPY) production in rats' brains and a decrease in leptin concentrations in their bloodstream.

"Very likely, this is part of human clinical pathology, like that in teen-age anorexia or loss of appetite in the elderly," said Shay, a professor of nutritional biochemistry. "We are certainly not saying that this is a cause of anorexia, but these findings hint at exacerbating or accelerating factors. If a teen-ager eliminates key foods from her diet, for example, she eventually could become zinc deficient."

Zinc is an essential trace mineral readily accessible by eating red and white meat and shellfish. In addition to leading to anorexia, chronic zinc deficiency can result in reduced growth and sexual development, a weakened immune system, hair loss and skin lesions.

"For people trying to recover from anorexia, or those who are having trouble holding onto body weight, I believe our work strengthens earlier findings that recommend the use of zinc supplements," Shay said. "Another lab has shown that zinc supplements have led to greater recovery rates."

The increase in the production of NPY, a compound that is 36 amino-acids long and found in brain tissue, came as a mild surprise, Shay said. Since the compound had been recognized for its role in stimulating appetite, he had theorized a decline in its production in times of zinc deficiency. Instead production increased but the compound failed to produce its appetite-stimulating effect. New experiments are under way in Shay's lab -- among only a handful studying NPY during nutritional deficiencies -- to determine the cellular makeup of the compound to find out why it becomes inactive.

Like NPY, the hormone leptin, which is made in fatty tissue and released into the bloodstream, has been shown to have potent effects on body weight and food-intake. Shay has found that when zinc deficiency occurs, stores of leptin decline significantly in rats. Similar unpublished work on humans, reported by Shay at Experimental Biology 1998 in April in San Francisco, has yielded similar results.

During zinc deficiency-induced anorexia, the researchers reported in Nutritional Biochemistry, circulating leptin concentrations are low and should stimulate an increase in NPY if the leptin-NPY link is functional. Shay theorizes that zinc deficiency affects the processing capabilities of NPY and negatively impairs its normal appetite-stimulating effect.

University of Illinois at Urbana-Champaign

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