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The effect of zinc deficiency on the growth promoting effect of circulating IGF-I and the direct growth effect of GH on long bone growth were investigated. Food intake was decreased by lack of zinc in the diet. Tissue zinc content and plasma alkaline phosphatase activity were reduced by zinc deficiency. Systemic administration of human IGF-I increased the body weight, tail length and tibia epiphyseal cartilage width of control animals. This somatogenic action was impaired by zinc deficiency, as evidenced by continued weight loss, no increase in tail length and decreased tibial epiphyseal cartilage width of zinc deficient animals. Unilateral arterial infusion of GH increased the tibial epiphyseal width of the treated limb but not of the non-treated limb in control rats. However, no difference was found between the infused and the non-infused limb of zinc deficient animals, suggesting the occurrence of GH resistance on long bone growth in zinc deficiency. We conclude that zinc deficiency inhibits the growth promoting action of circulating IGF-I and the direct growth effect of GH on long bone growth.

The effect of low dietary zinc on the survival and reproduction of an intestinal nematode (Heligmosomoides polygyrus) during both primary (Experiment 1) and challenge (Experiment 2) infections was investigated. Plasma zinc concentrations were significantly lower in mice fed a 5 ppm zinc diet (ZR), compared with control mice fed a 60 ppm zinc diet (C) in both experiments. There were no significant differences between ZR and C mice in any other zinc parameter or on worm burdens or worm fecundity in either experiment. Comparisons between the primary infection and the challenge infection did suggest a possible effect of calorie restriction on worm burdens. / Parasitic infection did, however, affect the host nutritional status. Spleen weight was significantly higher in infected mice in both experiments. In the challenge infection, both liver and spleen copper concentrations were significantly higher, and spleen iron concentration significantly lower in the infected mice. That these significant results were seen only in the challenge infection may suggest the role of the host immune response.

Interactions among zinc deficiency, energy restriction, immunity and Heligmosomoides polygyrus (Nematoda) infection in mice were investigated. Mice were fed zinc-sufficient (Zn+: 60mg zinc/kg diet), zinc-deficient (Zn$-$: 0.75 mg/kg) or pair-fed (PF) diets. Liver and serum zinc concentrations were reduced in Zn$-$ mice, but zinc content of worms was unaffected by host diet. Both zinc deficiency and energy restriction accelerated worm maturation during a primary infection, but zinc deficiency caused stunting of female worms. Energy restriction led to a anteriorad distribution of worms along the intestine whereas zinc deficiency led to a posteriorad distribution. Enhanced parasite survival in Zn$-$ and PF mice was associated with a decreased immune response in both primary and challenge infections. In the primary infection, spleen cell production of interleukin-4 (IL-4) and interferon-gamma (IFN-$ gamma$), peripheral eosinophilia and serum levels of IgE and IgG1 were reduced by zinc deficiency, whereas the reduced delayed type hypersensitivity (DTH) response and impaired interleukin-5 (IL-5) production were attributed to energy restriction. In the challenge infection, reduced antibody levels (total IgE and IgG1, parasite-specific IgG1 and IgG3) and eosinophilia were attributed to zinc deficiency whereas the higher worm numbers were attributed to a combined effect of zinc deficiency and energy restriction. Although the absolute number of spleen cells was reduced in both Zn$-$ and PF mice, neither deficiency altered the proportion of the cell subpopulations. In vitro functional assays in response to parasite antigen (Ag) revealed that T cell proliferation was reduced by a direct effect of zinc deficiency on T cells, and by the effects of energy restriction on antigen presenting cells (APC). Impaired cytokine production in Zn$-$ mice was more complex. Zinc deficiency reduced T cell function (IL-4 production), energy restriction decreased T cell (IFN-$ gamma$ productio

Experiments were conducted with sows and littermate-gilts to investigate the effect of dietary zinc (Zn) restriction during either part or most of the pregnancy and lactation on dams and their offspring. / Reduced dietary Zn (13 ppm) during the last 4 wk of pregnancy and first 2 wk of lactation presented no serious consequences to the dam or offspring. Reduction of dietary Zn throughout pregnancy and lactation (10 ppm) caused overt signs of Zn deficiency in one-half of the gilts, however, their offspring exhibited no obvious abnormalities. Zinc restriction did not affect feed consumption but depressed plasma and urinary Zn and plasma alkaline phosphatase activity (APA). The use of the balance technique and radiotracers revealed that gilts deficient in Zn initiated protective mechanisms such as, increased Zn absorption reduced endogenous Zn excretion, prolongation of the biological half life of Zn; all these responses affected higher efficiency of Zn utilization. / Despite the protective mechanisms, gilts depleted in Zn exhibited prolonged stressful parturition and a high incidence of intrapartum and neonatal mortality than control gilts. Piglets from gilts depleted in Zn showed depressed birth weight, reduced concentrations of plasma Zn, Cu and ammonia and low APA and hematocrit, increased plasma concentrations of glucose and lactate, reduced content of Zn in liver, heart, lung, skin, bone and carcass and higher concentrations of Cu and Mn in various tissues compared to controls. Zinc depletion did not change the Zn content of colostrum but did change it in milk. Content of Cu, Fe, and Mn was effected in colostrum and milk. Weight of piglets was lower at one wk but not at two wk of age. Two-week old piglets exhibited lower Zn and higher Cu concentrations in plasma; reduced Zn and increased Cu and Mn concentrations in liver and bone and changes in Cu and Mn in other tissues. At the end of lactation, gilts depleted in Zn exhibited low level of Zn and APA in plasma; reduced Zn content in liver, spleen, heart, small intestine; increased Cu content in liver and small intestine; increased Zn and Mn content in brain. / Although gilts depleted in Zn exhibited a highly efficient handling of Zn via homeostatic mechanisms, the reduced amount of corporal exchangeable Zn in these gilts caused biochemical changes affecting the performance of the dam and the offspring. (Abstract shortened with permission of author.)

Corrigenda tipped to title page. / Includes bibliographical references (leaves 313-353). / xxvii, 353 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Investigates the iron status and dietary intakes in 6-24 month old children in Australia and Ghana and assesses the effects of dietary calcium on intestinal iron absorption. The true prevalence of non-anaemic iron deficiency (NAID) and iron deficiency anaemia (IDA) and dietary intakes in infants and toddlers from a broad socio-economic background were assessed by haematological and biochemical parameters, semi-quantitative diet recall and anthropometric measurements. The high prevalence of iron deficiency and anaemia found in Australian and Ghanaian children can be attributed to the low intake of bioavailable iron in weaning diets which are often ingested with large amounts of calcium. While calcium has been shown to inhibit the absorption of iron, its mechanism of interaction with iron absorption at the intestinal level is not known. The rat was used as an experimental model to investigate the effects of dietary calcium on duodenal iron uptake. The results indicate there is a critical period during weaning when the consumption of high dietary calcium with low iron can retard growth potential. Dietary calcium significantly inhibits non-haem iron absorption at the intracellular level by up-regulating villus enterocyte ferritin concentrations under iron deficiency conditions. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1998

Thesis (M.S.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on January 8, 2008) Includes bibliographical references.

Thesis (Ph. D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on January 3, 2008) Includes bibliographical references.

Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1998? / Corrigenda tipped to title page. Bibliography: leaves 313-353.

Thesis (M.Sc.)--University of Adelaide. / Typewritten copy.