Diets, lead

Given drinking water with 10 mg Pb/L for 51 days diets were either low in calcium (0.3% Ca) or adequate in calcium (3% Ca) Birds given low calcium diets accumulated up to 4 times more lead in tissues than finches on high calcium diets. Lead concentrations in mg/kg DW for low Ca vs. high Ca diets were 2.4 vs. 0.6 in liver, 4.9 vs. 1.5 in kidney, and 48 vs. 8 in bone 52... 

The presence of S. mutans and other cariogenic bacteria contributes towards the formation of a biofilm known as dental plaque, and their metabolism of fermentable carbohydrates in the diet leads to the formation of acids [12]. Dental caries has been described as a complex imbalance in physiologic equilibrium between tooth mineral and biofilm [13]. Biofilms imply the involvement of microbiological species [14], but the key concept included within this definition is that the bacteria involved are native to the body, not a group of specific invasive bacteria causing infection [14]. 

The pyruvate decarboxylase reaction provides our first encounter with thiamine pyrophosphate (TPP) (Fig. 14-13), a coenzyme derived from vitamin B Lack of vitamin Bi in the human diet leads to the condition known as beriberi, characterized by an accumulation of body fluids (swelling), pain, paralysis, and ultimately death. 

Vitamin D3 is a precursor of the hormone 1,25-dihy-droxyvitamin D3. Vitamin D3 is essential for normal calcium and phosphorus metabolism. It is formed from 7-dehydrocholesterol by ultraviolet photolysis in the skin. Insufficient exposure to sunlight and absence of vitamin D3 in the diet leads to rickets, a condition characterized by weak, malformed bones. Vitamin D3 is inactive, but it is converted into an active compound by two hydroxylation reactions that occur in different organs. The first hydroxylation occurs in the liver, which produces 25-hydroxyvita-min D3, abbreviated 25(OH)D3 the second hydroxylation occurs in the kidney and gives rise to the active product 1,25-dihydroxy vitamin D3 24,25 (OH)2D3 (fig. 24.13). The hydroxylation at position 1 that occurs in the kidney is stimulated by parathyroid hormone (PTH), which is secreted from the parathyroid gland in response to low circulating levels of calcium. In the presence of adequate calcium, 25(OH)D3 is converted into an inactive metabolite, 24,25 (OH)2D3. The active derivative of vitamin D3 is considered a hormone because it is transported from the kidneys to target cells, where it binds to nuclear receptors that are analogous to those of typical steroid hormones. l,25(OH)2D3 stimulates calcium transport by intestinal cells and increases calcium uptake by osteoblasts (precursors of bone cells). 

The serum concentration of calcitriol varies inversely with phosphate throughout the day. Feeding subjects on low phosphate diets leads to a fall in serum phosphate and an increase in circulating calcitriol. It is not clear whether or not this is a direct effect of phosphate on the kidney hydroxylases. 

The main effect of riboflavin deficiency is on lipid metabolism. In experimental animals on a riboflavin-free diet, feeding a high-fat diet leads to more marked impairment of growth, and a higher requirement for riboflavin to restore growth. There are also changes in the patterns of long-chain polyunsaturated fatty acids in membrane phospholipids. 

Ascorbic acid. Vitamin C, is a water-soluble vitamin of great im-portance. A deficiency of vitamin C in the diet leads to scurvy, a disease characterized by loss of weight, general weakness, hemorrhagic condition of the gums and skin, loosening of the teeth, and other symp-toms. Sound tooth development seems to depend upon a satisfactory supply of this vitamin, and a deficiency is thought to cause a tendency to incidence of a number of diseases. 

Mwy of the effects of leukotrienes are reduced in animats raised cm diets deficient in essentia] fatty adds. Such diets lead to a reduction in all the functions of the essential fatty acids. The advantage of drugs is that they can be designed to affect specific functions of the EFAs rather than all functions. 

Free sulfate occurs in the plasma at concentrations of 1 to 2 mAf, The sulfate in the plasma and glomerular filtrate has been a concern for those interested in calcium status. Consumption of high-protein diets leads to increases in urinary calcium levels. This effect has been attributed, in part, to the catabolism of sulfur amino adds to yield free sulfate. The sulfate forms a complex with the calcium in... 

In the second case, the authors were unsure if the associated graft failure was due to the acute metabolic acidosis or thiamine deficiency, since the absence of thiamine in the diet leads to poor glucose oxidation, resulting in accumulation of lactic acid and metabolic acidosis, which is refractory to any treatment except thiamine supplementation. 

The nature of the complexes formed between AP+ and citrate is important because even though citrate may not be a substantial binder of AP+ in plasma, it can help AP+ cross membranes. This may occur both for AP+ transport within the body and for AP+ uptake from the gut. For example, citrate in the diet leads to enhanced AP+ levels in the brain and bones of rats 124), and to enhanced blood levels in humans taking Al(OH)3-based antacids together with citrate (125). 

In keeping with the presumed importance of serotonin in the pathophysiology of BN is the finding that a reduction in the synthesis of serotonin in the brain, brought about by a diet deficient in tryptophan, precipitates a loss of eating control and an increased concern with body image in recovered BN patients (Smith et al. 1999). Chronic depletion of plasma tryptophan may be one of the mechanisms by which dieting leads to the development of BN in vulnerable subjects. 

Strict adherence to a gluten-free diet leads to mucosal recovery in celiac disease and reduces the risks of bowel malignancy. TGA can be used as a marker for monitoring dietary compliance in addition to its diagnostic role. ... 

Consumption of mercury in the diet leads to the accumnlation of this metal in the body (Figure 15). 

In clot formation, molecules of the serum protein prothromhin must be activated to produce thrombin, which then initiates the final stages of clot formation. This requires binding of Ca + ions to the unusual amino acid 7-carboxyglutamate in prothrombin. Vitamin K is required as a coenzyme by the enzyme that adds the carboxyl groups to the normal amino acid glutamate to form 7-carboxyglutamate. Thus a deficiency of vitamin K in the diet leads to poor blood clotting. 

A high-protein diet leads to increased production of urea. Drinking more water increases the volume of urine, ensuring elimination of the urea from the body with less strain on the kidneys than if urea were at a higher concentration. 

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