The human gastrointestinal system can absorb 30-40% of ingested copper from the typical diets consumed in industrialized countries. Experimental data support the existence of a carrier-mediated transport mechanism with an affinity constant in the micromolar range. Aging probably decreases the efficiency of copper homeostasis, resulting in higher plasma copper concentrations in the elderly. Physiologic differences may account for the higher cupremia of females. Supplements of minerals with similar chemical characteristics could reduce copper absorption. This property has pharmacologic applications in Wilson disease. Manipulation of the fiber content of the diet may have an indirect effect on copper bioavailability by altering the bioavailability of mineral antagonists. Proteins and soluble carbohydrates tend to improve copper absorption and bioavailability by enhancing its solubility and intestinal bulk flow. Organic acids, other than ascorbic acid, or agents that form low-molecular-weight chelates, are likely to have a positive effect on overall copper absorption. Conditions associated with malabsorption of macronutrients and gastrointestinal disease can impair copper uptake and contribute to suboptimal copper status.
Recent clinical and experimental findings have reinforced the link among zinc deficiency, malnutrition and diarrheal disease. Because there is a strong association between protein and zinc content in virtually all types of foods, insufficient protein intake may often be the cause of zinc deficiency. Compensatory mechanisms operating in monogastric species during malnutrition are less effective for the absorption of transition divalent elements such as zinc, which remain bound to ligands of dietary or endogenous origin. Both protein and zinc deficiencies are strong negative determinants for normal cellular immunity. In zinc deficiency, the organism is more susceptible to toxin-producing bacteria or enteroviral pathogens that activate guanylate and adenylate cyclases, stimulating chloride secretion, producing diarrhea and diminishing absorption of nutrients, thus exacerbating an already compromised mineral status. In addition, zinc deficiency may impair the absorption of water and electrolytes, delaying the termination of normally self-limiting gastrointestinal disease episodes. The gastrointestinal tract may be one of the first target areas where zinc insufficiency may be manifested. A prolonged low zinc intake deprives the organism of the local potential beneficial effects of zinc, including interactions with oxidative free radicals and nitric oxide metabolism. Nitric oxide is a second messenger that plays an important part in the triggering of diarrheal disease. The possible interrelationship among infection, inflammation, free radical damage and its quenching by potential scavengers, such as zinc, in the intestinal lumen or within the enterocyte should be more extensively studied.
ABSTRACT. We studied the effect of early weaning from maternal breast milk to artificial diets on rat jejunal absorption of an exogenous 40-kD glycoprotein, horseradish peroxidrse (HRP). Rat (8-1 2). The effects of diet and nutritional factors on the normal development of the gastrointestinal macromolecular barrier are incompletely understood. Formula feeding~, in contrast to MM, have been reported to lead to increases in intestinal permeability in human infants, newborn rabbits, and guinea pigs ( 1 1, 12). In humans, the use of small molecule, nonmetabolizable markers limits the relevance to rnacrornolecubr absorption (12-14). In the rabbit, no artificial-feeding permeability-damaging factor has been isolated, and no immunologic mechanism accounting for the increased absorption demonstrated (1 I). Although it could turn out that normal closure requires the continuous p r a n c e of MM-derived trophic or hormonal factors, no experimental evidence for such a mechanism has been reported (7). Some evidence does suggest a possible role for endogenous glucocorticoids in this proces in rats (1, 9, 10, I S , 16).We evaluated the effect of early weaning to formula feedings
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