Zinc deficiency teratogenicity: the protective role of maternal tissue catabolism.

The effect of maternal metabolic state on the response to dietary zinc deficiency was assessed with the pregnant rat as a model. Sprague-Dawley rats were fed from mating to term: 1) a zinc-adequate (100 micrograms/g) control diet ad libitum, or 2) a zinc-deficient diet (0.7 micrograms/g) ad libitum, or 3) a control diet at reduced intake, or 4) a zinc-deficient diet at reduced intake, or 5) a zinc-deficient diet ad libitum plus additional zinc-deficient diet, fed by intubation, to maintain total intake at approximately 14 g/day. Dams receiving the zinc-deficient diet deposited more zinc (240-330%) into the products of conception than was consumed, showing that tissue catabolism is a substantial source of zinc. In rats fed the control diet ad libitum only 3% of the zinc consumed was deposited into the products of conception. Litters from dams fed the deficient diet at restricted levels (resulting in greater tissue catabolism) had fewer malformations and resorptions than litters from dams fed the zinc-deficient diet ad libitum. Maintenance of total intake of the zinc-deficient diet at 14 g/day by intubation resulted in a pronounced drop in voluntary intake. By day 18 of pregnancy voluntary intake had almost ceased, following day 18 the rats became severely distressed if any zinc-deficient diet was force-fed. Rats fed the zinc-deficient diet ad libitum also displayed a dramatic fall in voluntary intake after day 18 of gestation. These data show that the reduction in food intake during zinc deficiency is not due to gustatory influences alone and that metabolic state, defined as the balance between anabolism and catabolism, is a critical factor in determining the availability of zinc to the litter during zinc deficiency.