Neonatal dietary zinc deficiency in artificially reared rat pups retards behavioral development and interacts with essential fatty acid deficiency to alter liver and brain fatty acid composition

Abstract

The objective of this study was to investigate whether short-term zinc deficiency in the early neonatal period would exacerbate the effects of essential fatty acid (EFA) deficiency on liver and brain long-chain polyunsaturated fatty acid (LCPUFA) composition, as well as on behavioral development in artificially reared rat pups. Using a 2 x 2 factorial design, male Long-Evans rat pups were reared artificially from postnatal d 5 to 16; pups were fed through gastrostomy tubes with rat formula deficient in zinc and/or EFA. As expected, EFA deficiency significantly reduced levels of arachidonic acid [AA, 20:4(n-6)] and docosahexanoic acid [DHA, 22:6(n-3)] in liver phosphatidylcholine (PC) and brain phosphaditylethanolamine (PE), and increased 22:5(n-6) levels in liver and brain PC and PE. There were significant interactions between zinc and EFA in liver such that zinc deficiency reduced AA and DHA in the EFA-adequate groups, but significantly increased AA in the EFA-deficient groups. Contrary to the hypothesis, short- term zinc deficiency did not exacerbate the effects of EFA deficiency in liver phospholipids. In brain PE, a significant interaction between EFA and zinc was observed such that zinc deficiency increased 22:5(n-6) concentrations in EFA-adequate but not in EFA-deficient groups. Regardless of their EFA status, zinc-deficient rats were growth retarded and demonstrated deficits in locomotor skills. Possible effects of long-term zinc and EFA deficiency on brain function should be investigated in future studies.