Development of zinc deficiency in ⁶⁵Zn labeled, fully grown rats as a model for adult individuals

The development of zinc deficiency in adults was studied in a metabolism experiment involving 31 adult, female rats labeled homogenously with ⁶⁵Zn. The animals were fed restricted amounts (8 g/day) of a semisynthetic diet containing either 58 μg Zn/g (control, n = 7) or 2 μg Zn/g (Zn deficiency, n = 24). Control animals were sacrificed at day 0 (n = 3) and day 29 (n = 4). Zinc deficient animals were sacrificed at day 1, 2, 4, 7, 11, 16, 22, and 29 (3 animals per group). The development of zinc deficiency comprised 4 phases: (I) Fecal Zn excretion needed several days to adjust to the low level of Zn intake. The high initial Zn loss via feces was counterbalanced mainly by Zn mobilization from the skeleton. (II) During the 2^nd week of deficiency Zn mobilization from tissue storage changed transiently to soft tissues (mainly muscle and fat tissue). (III) After the 2^nd week the skeleton resumed to mobilize Zn. (IV) At the end of the study the skeleton Zn storage was exhausted and alkaline phosphatase activity indicated severe Zn deficiency. Urinary Zn excretion was too small to contribute quantitatively to changes in Zn metabolism during any phase of Zn deficiency. In conclusion, adults may compensate a deficient Zn supply by mobilizing tissue Zn for several weeks. The skeleton revealed to be the major short-term as well as long-term source of whole body tissue Zn that can be mobilized.