Changes in hypothalamic noradrenergic systems during the anorexia of zinc deficiency

Anorexia and altered patterns of food ingestion are an early manifestation of dietary Zn deficiency. In these experiments, the relationship between hypothalamic neurotransmitter systems and aberrant feeding behaviors was investigated. The concentration of tyrosine, DOPA, dopamine, norepinephrine (NE), epinephrine, tryptophan, serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA), as well as monoamine oxidase A (MAO-A) activity, were measured in the hypothalamus of rats fed Zn-restricted diets for 6 wk from weaning and compared to either Zn-supplemented pair-(semistarved) and ad libitum-fed controls. In Zn-deficient rats, NE increased 30%, MAO-A rose 20%, and other transmitters were unchanged, compared to either Zn-adequate control group. In adult rats acutely deprived of dietary Zn, cyclic feeding patterns ensued only after a 4-d lag period, during which time hypothalamic NE was not changed, despite an approximately 50% reduction in plasma Zn. These data suggest that elevations in NE do not function as a signal to initiate a reduction in food intake, but rather represent a compensatory attempt to stimulate feeding. We propose that during Zn deficiency, a reduction in the receptor affinity for NE may occur and might represent the primary deficit responsible for reduced food intake in this condition.