Intestine treated dietary protein

In patients with renal failure, the occurrence of conditioned zinc deficiency may be the result of a mixture of factors, which at present are ill defined. If 1,25-dihydroxycholecalciferol plays a role in the intestinal absorption of zinc, an impairment in its formation by the diseased kidney would be expected to result in malabsorption of zinc. It seems likely that plasma and soft tissue concentrations of zinc may be "protected in some individuals with renal failure by the dissolution of bone which occurs as a result of increased parathyroid activity in response to low serum calcium. In experimental animals, calcium deficiency has been shown to cause release of zinc from bone. In some patients who are successfully treated for hyperphosphatemia and hypocalcemia, the plama zinc concentration may be expected to decline because of the deposition of zinc along with calcium in bone. Thus, in the latter group in particular, a diet low in protein and high in refined cereal products and fat would be expected to contribute to a conditioned deficiency of zinc. Such a diet would be low in zinc. The patients reported by Mansouri et al. (37), who were treated with a diet containing 20-30 g of protein daily and who had low plasma concentrations of zinc, appear to represent such a clinical instance. Presumably the patients of Halsted and Smith (38) were similarly restricted in dietary protein. In other patients with renal failure whose dietary protein was not restricted, plasma zinc concentration were not decreased. Patients on dialysis had even higher levels, particularly... 

In vivo studies using mouse models have proved that curcumin modifies apoptosis resistance, leading to the inhibition of tumor formation and the prevention of adenoma development in the intestinal tract. The chemopreven-tive effect of curcumin for intestinal tumors in Min/+ mice was investigated. A dietary level of 0.15% curcumin decreased tumor formation in Min—/— mice by 63%. Examination of intestinal tissue from the treated animals showed the tumor prevention by curcumin was associated with increased enterocyte apoptosis and proliferation. Curcumin also decreased expression of the oncoprotein (S-catenin in the erythrocytes of the Min/+ mouse, an observation previously associated with an antitumor effect. Curcumin enhanced PhlP-induced apoptosis and inhibited PhIP-induced tumorigenesis in the proximal small intestine of Ape (min) mice. Experiments performed on intestinal tumors in C57BL/6J-Min/+ (Min/+) mice demonstrated that curcumin has a regulatory role in lymphocyte-mediated immune function [Churchill et al., 2000]. Furthermore, levels of COX-2 protein expression have been found to reflect the retardation of adenoma development in mouse intestines after treatment with curcumin [Tunstall et al., 2006]. 

Kameoka S, Leavitt P, Chang C, Kuo SM. Expression of antioxidant proteins in human intestinal Caco-2 cells treated with dietary flavonoids. Cancer Lett 1999 146 161-167. 

The effect of dietary wheat bran and dehydrated citrus fiber at 15% level and 5% dietary fat on intestinal carcinogenesis induced by AOM and DMAS was studied in male F344 rats (44,45). Composition of diets was adjusted so that all animals in different experimental groups consumed approximately the same amount of protein, fat, minerals and vitamins. The animals fed the wheat bran or citrus fiber and treated with AOM had a lower Incidence (number of animals with tumors) and multiplicity (number of tumors/tumor bearing rat) of colon tumors and tumors of the small Intestine than did those fed the control diet and treated with AOM (Table II 15). Although 15% purified pectin in the diet (41) inhibited the colon tumor incidence better than did 15% dehydrated citrus fiber, in this study the Inhibition of colon tumor multiplicity was more pronounced with the dehydrated citrus fiber compared with purified pectin. Because dehydrated citrus fiber contains about 20% pectin, the pectin content of this diet was considerably lower than that of the diet used in... 

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