Calbindin formation

Seress L, Gulyas Al, Ferrer I, Tunon T, Soriano E, et al. 1993. Distribution, morphological features, and synaptic connections of parvalbumin- and calbindin D28k-immunoreactive neurons in the human hippocampal formation. J Comp Neurol 337 208-230. 

Children are particularly vulnerable to excess strontium because the immature skeleton has a high rate of bone remodeling, and strontium adversely affects bone development in several ways, as demonstrated in animal studies. In chickens and rats, excess strontium suppresses the activation of vitamin D3 in the kidney, which severely reduces the expression of calbindin D mRNA and the translation of calbindin D protein in the duodenum (Armbrecht et al. 1979, 1998 Omdahl and DeLuca 1972). As a result, duodenal absorption of calcium is reduced. Strontium also binds directly to hydroxyapatite crystals, which may interfere with the normal crystalline structure of bone in rats (Storey 1961). In addition, excess strontium may prevent the normal maturation of chondrocytes in the epiphyseal plates of long bones of rats (Matsumoto 1976). Excess strontium apparently interferes with the mineralization of complexed acidic phospholipids that is thought to help initiate the formation of hydroxyapatite crystals in developing bone (Neufeld and Boskey 1994). As a result, affected bone contains an excess of complexed acidic... 

This active vitamin D metabolite (1,25 dihydroxycholecalciferol) is an important cofactor for intestinal calcium absorption, which involves calbindins (calcium binding proteins) in the intestine and kidney. Calcitriol is produced in the kidneys by the conversion of 25-hydroxycholecalciferol (calcidiol) and its formation is stimulated by a reduction of plasma calcium and/or phosphate and increased production of parathyroid hormone and prolactin (Figure 6.3). Calcitriol also inhibits the release of calcitonin and, together with PTH, increases the absorption of calcium and phosphate from the gastrointestinal tract and the kidneys. Growth hormone, glucocorticoids, estrogens, testosterone, and the thyroid hormones also influence calcium metabolism. 

Vitamin D is required for efficient absorption of calcium and phosphorus in the intestinal trad, and it is also necessary for calcium and phosphorus homeostasis within the body. Deficiency of vitamin D will, therefore, lead to calcium deficiency and will affect processes such as bone formation and egg-shell production. Bone mineralisation is dependent on the maintenance of Gi and phosphate levels. The effect of vitamin D on these processes is mediated by calbindin and is discussed in Section 10.6. Aluminium toxicity is, at least in part, accounted for by disturbance of calcium homeostasis. Aluminium compounds reduce vitamin D-dependent Gi absorption in chicks. They act by reducing the intestinal calbindin concentration (Dunn et al, 1993). 

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