Calcium is absorbed in the duodenum and jejunum in the form of calcium ions. The absorption direction of calcium is from the side of the small intestine mucosa and then from the serosal side. There are three main ways: 1) actively traversing the cells, including calcium ions diffusing into the cells through the chorion, moving in the cytoplasm, and from the cells. Introgression of extracellular cells; 2) Intercellular transfer of calcium ions, which works only when the concentration of calcium ions in the small intestine is sufficiently high; 3) through the cellarization and exocytosis of the cells. When calcium ions enter the small intestine cells, energy is no longer needed by the electrochemical gradient. Intracellular calcium ions are transferred in the form of calcium binding protein, free calcium ions and calcium ion vesicles. When calcium ions ooze out from the cells to the outside of the cells, the calcium in the calcium ion-binding protein is discharged by the calcium pump; the free calcium is exchanged with sodium-potassium for calcium ion exchange; the calcium bubble which enters the cells by the pinocytosis is released by exocytosis. calcium. The intercellular transfer of calcium depends on the degree of junction between the cell membranes, and some amino acids such as lysine can constitute intercellular calcium ion transfer.
During the absorption of calcium, vitamin D3 is essential for the absorption of calcium, as active vitamin D3 (1,25-(OH)2-VD3) is involved in the synthesis of calcium-binding proteins in small intestinal mucosal cells. Vitamin D3 also promotes the flow of calcium ions between cells. High phosphorus, high magnesium, high zinc, high oxalic acid and high phytic acid in the diet interfere with the absorption of calcium; citric acid, lactose and sucrose can improve the absorption of calcium; excessive fat or fat indigestion in the diet can form Insoluble calcium soap, which reduces the absorption of calcium.
During calcium metabolism, calcium homeostasis is regulated by a number of factors including dietary calcium, phosphorus levels, vitamin D, parathyroid hormone (PTH), and calcitonin. Calcium intake affects calcium absorption and bone resorption through the regulation of PTH and vitamin D metabolites. Low-calcium diets result in increased calcium absorption because low diets tend to plasma calcium, thereby increasing PTH release. PTH promotes the conversion of kidney 25-hydroxycalciferol to 1,25-dihydroxycalciferol, resulting in enhanced calcium absorption. The regulation of circulating levels of calcium in the blood depends on the secretion of PTH and calcitonin, which control the deposition and reabsorption of bone calcium. Eating low-calcium diet, plasma low calcium, stimulate the secretion of PTH, thereby promoting the release of bone calcium and phosphorus, to meet the needs of calcium in the body, and phosphorus is discharged; eating high-calcium diet will inhibit the use of bone calcium. Therefore, calcium and phosphorus in the bone are in dynamic equilibrium, which often manifests as deposition and reabsorption of bone calcium and phosphorus. Calcium excretion in pigs is mainly excreted from the feces, including calcium that has not been digested and absorbed, and endogenous fecal calcium. The amount of calcium excreted in pigs is small, but it still reflects the retention and utilization of calcium. Pig metabolized fecal calcium is 0.0322g, and endogenous urinary calcium is 1% of fecal calcium.
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