Zinc and Hormones
Zinc deficiency affects hypothalamic pituitary thyroid function. Thyrotropin releasing hormone content was decreased in the zinc deficient rat (Morley et al., 1980). Ultimately triiodothyronine (T3) and thyroxin levels were decreased. The hypothalamic axis susceptibility to Zn deficiency may explain the dynamic relationship between testosterone and Zn. Injections of testosterone or dihydro-testosterone in mice restores normal zinc content (Donovan and Thomas, 1980) while Zn deficiency decreases serum production and delays puberty (Prasad, 1966).
Elevations in hypothalamic Zn concentrations in the rat appear to correlate with the release of gonadotropin releasing hormone and gonadotropins which occurs between proestrus and estrus and after castration, although this, of course, does not establish a causal relation (Zinc and Manganese in the Schizophrenias
Merriam et al., 1979). Hypothalamic Zn ions rise with gonadotropin secretions (Merriam et al., 1979; Root et al., 1979). Hypogonadism occurs with Zn deficiency (Caggiano et al., 1969; Prasad, 1966).
Zinc deficiency inhibits essential fatty acid metabolism to prostaglandins (PG) either by blocking linoleic acid desaturation to gamma - linoleic acid or by inhibiting mobilization of dihomo - gamma linolenic acid from tissue membrane stores (Cunnane and Horrobin, 1980). Prolactin and Zn have similar actions on PGE1 formation and prolactin enhances flow of fluid from fetal to maternal compartments (Manku et al., 1975; Manku et al., 1979). Zinc deficiency can result in polyhydraminos (Manku et al., 1979). Opiates may have an effect on PGE1 synthesis which is opposite to that of Zn and there is evidence that reduced PGE1 production (possibly due to an endogenous opioid) may play a role in schizophrenia (Horrobin et al., 1978; Horrobin and Morgan, 1980). An enkephalin degrading amino peptidase from rat brain homogenates is a Zn metalloenzyme(Schnebli et al., 1979). A higher than normal proportion of arachidonate was found in the fatty acids of Zn deficient skin (Bettger et al., 1980). PGE2 and PGF2 have opposing effects on Zn transport and may act as regulators of the intestinal mucosa transport of Zn (Song and Adham, 1979).
Zinc deficiency and thyroid hormone shortage occurring in both cretinism and myxedema have similar signs, ie. retarded growth, reduced appetite and activity, impaired development of skin and hair (Hartoma et al., 1979). Zinc deficiency symptoms may be mediated by excess glucocorticoids since Zn depletion results in elevation of glucocorticoids. Elevated glucocorticoids and Zn deficiency both result in death of thymic lymphocytes (Donovan and Thomas, 1980). A deficiency of nerve growth factor may occur with Zn deficiency. One nerve growth factor is a small basic protein with three distinct types of sub-units (Vinores and Guroff, 1980). Two molecules of Zn are present in the complex and Zn participates in holding the structure together (Dunn et al., 1980; Pattison and Dunn, 1975). In the absence of Zn the subunits separate. Nerve growth factor is required for the survival and development of certain sympathetic and sensory neurons. It is equally clear that nerve growth factor affects a wide variety of other cells as well. Nerve growth factors are present on the plasma membrane and almost certainly at the synaptic ending as well (Dunn et al., 1980). Nerve growth factor action increased dendritic attachments which requires elevated levels of RNA synthesis, which is Zn dependant.
- From article on
Zinc and Manganese in the Schizophrenias by Carl Pfeiffer
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