Calcium-deficient diet

Ishida et al., 1998 9 week old OVX rats calcium-deficient diet daidzin 10, 25, 50 mg/kg bw by gavage treatment for 28 d starting 7 d after OVX High dose genistin or daidzin prevented bone loss. Daidzin retarded femoral bone loss in a dose-dependent manner... 

ISHIDA H, UESUGi T, HiRAi K, TODA T, NUKAYA H, YOKOTSUKA K and Tsuji K (1998) Preventive effects of the plant isollavones, daidzin and genistin, on bone loss in ovariectomized rats fed a calcium-deficient diet Biol Pharm Bulletin 21, 62-66. 

Iron appeared to reduce the effects of orally or subcutaneously administered lead on blood enzyme and liver catalase activity (Bota et al. 1982). Treatment of pregnant hamsters with iron- or calcium-deficient diets in conjunction with orally administered lead resulted in embryonic or fetal mortality and abnormalities (ranting, edema) in the litters, while treatment with complete diets and lead did not (Carpenter 1982). Inadequate levels of iron in association with increased body burdens of lead enhanced biochemical changes associated with lead intoxication (Waxman and Rabinowitz 1966). Ferrous iron was reported to protect against the inhibition of hemoglobin synthesis and cell metabolism by lead it has been speculated that iron competes with lead uptake by the cell (Waxman and Rabinowitz 1966). In... 

Deknudt G, Gerber GB. 1979. Chromosomal aberrations in bone-marrow cells of mice given a normal or a calcium-deficient diet supplemented with various heavy metals. Mut Res 68 163-168. 

For more than forty years, it has been known that increasing the protein content of the diet causes an increase in urinary calcium excretion (1, 2). There is, in fact, a direct correlation between urine calcium output and dietary protein level, so that excretion is 800 percent higher if dietary protein is increased from 6 g per day to 560 g per day (3 ). This relationship between urinary calcium and protein ingestion is not affected by the level of dietary calcium, and is evident even when severely calcium-deficient diets are consumed (3). 

Toda, T. et al.. New 6-0-acyl isoflavone glycosides from soybeans fermented with Bacillus subtilis (natto). I. 6-0-succinylated isoflavone glycosides and their preventive effects on bone loss in ovariectomized rats fed a calcium-deficient diet, Biological Pharmaceutical Bulletin, 22, 1193, 1999. 

The fact that vitamin D3 toxicity results from primarily uncontrolled intestinal calcium absorption suggests that it is dietary calcium and not vitamin D3 that exacerbates the hypervitaminosis D3 toxicity effect [119]. This was tested by the interaction of excess vitamin D3 and calcium restriction [113]. Rats fed a calcium-deficient diet and given 25,000 IU of vitamin D3 three dmes/week for 2.5 weeks did not succumb to overt hypervitaminosis D3. Simple calcium restriction increased intestinal but not renal 24-OHase activity, presumably because of the absence of parathyroid hormone regulation in the intestine [113]. Coupled with vitamin D3, excess intestinal 24-OHase increased several fold more. However, when dietary calcium was adequate, vitamin D3 excess increased intestinal 24-OHase activity only slightly because of a suppressive mechanism regulated in part by increased blood calcitonin [120],... 

Calcium Effects on Zinc Bioavailability for the Rat and the Human. It should be pointed out at this juncture that the nutrient requirement of calcium for the rat is much higher than for man. In fact, the molar ratio of calcium to zinc in excess of 660 1 is recommended for rat diets, while for man the ratio is between 80 1 and 160 1. To feed rats molar ratios of calcium and zinc similar to human requirements would necessitate either a very calcium deficient diet or one containing zinc at a level well in excess of the requirement. Neither choice is nutritionally suitable for demonstrating an effect of phytate on zinc availability. 

Moreover, myopathic Syrian hamsters given a calcium-deficient diet exhibit fewer lesions in skeletal and cardiac muscle (17). Conversely, facilitation of calcium uptake with ionophores or membrane-active toxins such as lysophospholipids or macrolide antibiotics accelerate necrosis of isolated skeletal muscle (19) and rat hepatocytes in culture (10). 

Both the synthetic analog, la-hydroxyvitamin D3 (7), and la,25-hydroxyvitamin D3 are potent stimulators of intestinal calcium absorption in organ culture 37, 58) in rats and chickens 26,36,69,145,146,198) fed vitamin D3 and calcium deficient diets. The ratio of activities of la-hydroxy- and la,25-dihydroxyvitamin D3 compared to the activity of vitamin D3 itself reaches 1000 in parathyroidectomixed-thyroidectomized animals 146). However, what these ratios mean as regards the therapeutic value of la-hydroxyvitamin D3 or la,25-dihydroxyvitamin D3 is not easy to assess. In clinical situations of impaired calcium utilization, there normally would be an adequate supply of calcium, phosphorous, and vitamin D3 in the diet. However, in certain metabolic dysfunctions (see Section 6) both la- and la,25-dihydroxyvitamin D3 have been clearly demonstrated to have therapeutic value. 

Structural chromosome aberrations, particularly chromatid gaps and increased frequency of fragment exchange, were observed in rat bone marrow cells after 14 days of exposure to 240 mg Zn/L drinking water (Kowalska-Wochna et al. 1988). Chromosomal aberrations were observed in bone marrow cells of mice fed diets equivalent to 650 mg Zn/kg BW daily, in mice exposed to zinc oxide by inhalation, and in mice maintained on a low-calcium diet (USPHS 1989). Aberrations in bone marrow of mice given 5000 mg Zn/kg diet may be associated with calcium deficiency (Leonard and Gerber 1989). Calcium is displaced by zinc in calcium-depleted conditions, leading to chromosomal breaks and interference in the repair process (USPHS 1989). 

Apparent absorption (intake minus fecal excretion) of calcium decreased when the diet contained muffins with added sodium phytate to increase the molar ratio of phytate/calcium from 0.04 to 0.14 and 0.24. One-half of the men excreted more calcium in feces than was consumed when the high phytate diet was consumed. People consuming diets with molar ratios of phytate/calcium exceeding 0.2 may be at risk of calcium deficiency because of low bioavailability of dietary calcium unless physiological adjustments can be accomplished that maintain homeostasis. 

Mineral deficiencies are not uncommon and can have quite a variety of causes—e. g., an unbalanced diet, resorption disturbances, and diseases. Calcium deficiency can lead to rickets, osteoporosis, and other disturbances. Chloride deficiency is observed as a result of severe Cr losses due to vomiting. Due to the low content of iodine in food in many regions of central Europe, iodine deficiency is widespread there and can lead to goiter. Magnesium deficiency can be caused by digestive disorders or an unbalanced diet—e.g., in alcoholism. Trace element deficiencies often result in a disturbed blood picture—i. e., forms of anemia. 

Protein or calcium deficiency impairs drug metabolism in animals, due to decreased activity of the microsomal enzymes of the liver. The sleeping time by hexobarbitone is increased as a result of prolonged protein malnutrition. Acetylsalicylic acid has been shown to be more toxic to animals on a diet deficient in protein and magnesium. 

Vitamin D deficiency (also calcium deficiency) produces a condition known in children as rickets and in adults as osteomalacia. The bones and teeth of children with rickets are poorly formed and soft. A child with rickets frequently has malformed limbs, especially bowlegs. Blood dotting may be impaired, and. in extreme cases, there may be disturbances of the nervous system. An improvement in the level of calcium in the diet, along with vitamin D or parathyroid extract when required, brings about a hardening of the bones, but leaves them misshapen if deformity has already occurred. 

Chronic calcium deficiency alone produced neurodegenerative effects, although neurofibrillary changes were most frequently seen in the monkey on a low calcium diet supplemented with aluminum and manganese. 

Phosphates are important because they affect the absorption of calcium and other elements. The absorption of inorganic phosphorus depends on the amount of calcium, iron, strontium, and aluminum present in the diet. Chapman and Pugsley (1971) have suggested that a diet containing more phosphorus than calcium is as detrimental as a simple calcium deficiency. The ratio of calcium to phosphorus in bone is 2 to 1. It has been recommended that in early infancy, the ratio should be 1.5 to 1 in older infants, 1.2 to 1 and for adults, 1 to 1. The estimated annual per capita intake in the United States is 1 g Ca and 2.9 g P, thus giving a ratio of 0.35. The danger in raising phosphorus levels is that calcium may become unavailable. 

A vitamin-deficient diet can result in lowered levels of plasma calcium however, the use of high-calcium diets during vitamin deficiency can result in the maintenance of normal plasma calcium levels. The requirement for the vitamin may be overridden, providing that the diet contains high levels of calcium. The physiologically important form of vitamin D, 1,25 dihydroxyvitamin Dj, is a hormone. Another hormone, parathyroid hormone (I TH), is used in the control of vitamin D metabolism and calcium levels, as detailed in the following sechon. 

FtCURE 9,54 Plasma calcium levels of rats fed (A) vitamin-deficient diets and (B) ejta-min-sufficient diets. (Redrawn with pGimission from Brommage and EteLuca, 1985.)... 

The data demonstrate that the vitamin-deficient rats (see Figure 9.54A) maintained near-normal levels of plasma calcium with the high-calcium diet, though not with the moderate- or low-calcium diets. The vitamin-sufficient rats (Figure 9.54B) maintained near-normal plasma calcium, even with the low-calcium diet. The study shows that normal levels of plasma calcium can be maintained with the high-calcium diet in the absence of the vitamin, whereas vitamin D was required to maintain plasma calcium with diets containing lower levels of calcium. 

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... 

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